Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2025.02.006
Like Xie , Sujun Xiao , Qinyi Zhou , Wang Chen , Zhihao Hu , Yunhui Li , Yizhou Liu , Xiaofeng Ma , Yuan Li
Background
Anticancer agent doxorubicin is essential for cancer treatment but often causes cardiotoxicity. Tectorigenin has shown potential cardioprotective effects, but underlying mechanisms remain unclear. We aimed to investigate whether Tectorigenin attenuates doxorubicin-induced myocardial injury.
Methods
Doxorubicin (DOX) was utilized in C57BL/6J mice and cardiomyocytes H9c2, to establish in vivo and in vitro cardiotoxicity models, then treated with Tectorigenin. The levels of ferroptosis-related factors were measured using specific assay kits. The Liperfluo and DHE stainings were used to detect levels of lipid ROS. Cardiac function in rats was assessed using echocardiography. Immunofluorescence staining was used to detect Nrf2 nuclear translocation. ELISA assay was employed to check serum CK-MB, BNP and Tn-T levels. Cardiac injury and fibrosis were evaluated through HE and Masson stainings. Furthermore, TEM was employed to observe mitochondrial ultrastructure. Western blot and immunofluorescence staining were utilized to detect protein levels.
Results
DOX induced ferroptosis in H9c2 cells concentration-dependently and time-dependently, which was alleviated by Tectorigenin treatment. ML385 or K67 abolished Tectorigenin's inhibition on DOX-induced H9c2 cell ferroptosis. Mechanistically, Tectorigenin promoted the expressions of p62 and p-p62, leading to decreased Keap1 expression. This cascade facilitated Nrf2 nuclear translocation and subsequently elevated HO-1 and GPX4 expressions. Moreover, Tectorigenin treatment improved cardiac function, myocardial injury, fibrosis and mitochondrial function in C57BL/6J mice induced by DOX, as well as ferroptosis.
Conclusion
Our findings reveal that Tectorigenin attenuates DOX-induced ferroptosis and myocardial damage by activating the p62-Keap1-Nrf2/HO-1/GPX4 axis, this may provide a therapeutic strategy for mitigating cardiotoxicity associated with chemotherapeutic agents.
{"title":"Tectorigenin attenuates myocardial damage by doxorubicin-induced ferroptosis by activating the p62-Keap1-Nrf2/HO-1/GPX4 axis","authors":"Like Xie , Sujun Xiao , Qinyi Zhou , Wang Chen , Zhihao Hu , Yunhui Li , Yizhou Liu , Xiaofeng Ma , Yuan Li","doi":"10.1016/j.jtcme.2025.02.006","DOIUrl":"10.1016/j.jtcme.2025.02.006","url":null,"abstract":"<div><h3>Background</h3><div>Anticancer agent doxorubicin is essential for cancer treatment but often causes cardiotoxicity. Tectorigenin has shown potential cardioprotective effects, but underlying mechanisms remain unclear. We aimed to investigate whether Tectorigenin attenuates doxorubicin-induced myocardial injury.</div></div><div><h3>Methods</h3><div>Doxorubicin (DOX) was utilized in C57BL/6J mice and cardiomyocytes H9c2, to establish <em>in vivo</em> and <em>in vitro</em> cardiotoxicity models, then treated with Tectorigenin. The levels of ferroptosis-related factors were measured using specific assay kits. The Liperfluo and DHE stainings were used to detect levels of lipid ROS. Cardiac function in rats was assessed using echocardiography. Immunofluorescence staining was used to detect Nrf2 nuclear translocation. ELISA assay was employed to check serum CK-MB, BNP and Tn-T levels. Cardiac injury and fibrosis were evaluated through HE and Masson stainings. Furthermore, TEM was employed to observe mitochondrial ultrastructure. Western blot and immunofluorescence staining were utilized to detect protein levels.</div></div><div><h3>Results</h3><div>DOX induced ferroptosis in H9c2 cells concentration-dependently and time-dependently, which was alleviated by Tectorigenin treatment. ML385 or K67 abolished Tectorigenin's inhibition on DOX-induced H9c2 cell ferroptosis. Mechanistically, Tectorigenin promoted the expressions of p62 and p-p62, leading to decreased Keap1 expression. This cascade facilitated Nrf2 nuclear translocation and subsequently elevated HO-1 and GPX4 expressions. Moreover, Tectorigenin treatment improved cardiac function, myocardial injury, fibrosis and mitochondrial function in C57BL/6J mice induced by DOX, as well as ferroptosis.</div></div><div><h3>Conclusion</h3><div>Our findings reveal that Tectorigenin attenuates DOX-induced ferroptosis and myocardial damage by activating the p62-Keap1-Nrf2/HO-1/GPX4 axis, this may provide a therapeutic strategy for mitigating cardiotoxicity associated with chemotherapeutic agents.</div></div>","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 573-581"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2024.07.006
Oluwafemi Adeleke Ojo , Musa Toyin Yakubu
Background and aim
Ethanolic extract of Trichilia prieureana leaves have been reported to exhibit anti-hyperglycemic activities without detailed information on the anti-diabetic activities. This study investigated the anti-diabetic activity of aqueous extract of T. prieureana leaves (AETPL) in type 2 diabetic (T2DM) male rats.
Experimental procedure
T2DM rats (induced with 10 % fructose solution ad libitum for 2 weeks and streptozotocin [STZ]; 40 mg/kg body weight {BW}) in groups B, C, D, E, and F were also administered distilled water (DW), metformin (100 mg/kg BW), 11.2, 22.3, and 44.6 mg/kg BW of AETPL, respectively, whilst non-diabetic rats in Group A received DW only (Sham Control, SC) for 14 days. The T2DM-related parameters were then evaluated.
Results
The fructose-fed streptozotocin-(FSTZ) treatment related significant (p < 0.05) increases in FBS, HbA1c, fructosamine, HOMA-IR, G6P, GP, TC, TG, LDL-C, urea, bilirubin, hepatic and pancreatic MDA levels; decreases in BW, serum insulin, creatinine, albumin, HOMA-β, glycogen, G6PD, HK, HDL-C, hepatic and pancreatic SOD, GPX, RG, catalase, Hb, PCV, MCH, MCHC, MCV, RBC, WBC, differentials and the destruction of the pancreatic β-cells, hepatocyte degeneration, and central hepatic vein congestion were reversed by AETPL, to values that compared well with SC in most cases. In the IpGGT model, the intraperitoneally administered AETPL reduced the blood glucose and elevated the plasma insulin levels. The AETPL at 44.6 mg/kg BW exhibited the most pronounced effects.
Conclusion
AETPL (44.6 mg/kg BW) restored T2DM-glycemic control and associated biochemical changes via up-regulation of insulin, carbohydrate metabolizing enzymes and restoration of pancreatic and hepatic histoarchitecture.
{"title":"Anti-diabetic activity of aqueous extract of Trichilia prieureana A. Juss leaves in fructose-fed streptozotocin-induced diabetic male Wistar rats","authors":"Oluwafemi Adeleke Ojo , Musa Toyin Yakubu","doi":"10.1016/j.jtcme.2024.07.006","DOIUrl":"10.1016/j.jtcme.2024.07.006","url":null,"abstract":"<div><h3>Background and aim</h3><div>Ethanolic extract of <em>Trichilia prieureana</em> leaves have been reported to exhibit <strong>a</strong>nti-hyperglycemic activities without detailed information on the anti-diabetic activities. This study investigated the anti-diabetic activity of aqueous extract of <em>T. prieureana</em> leaves (AETPL) in type 2 diabetic (T2DM) male rats.</div></div><div><h3>Experimental procedure</h3><div>T2DM rats (induced with 10 % fructose solution <em>ad libitum</em> for 2 weeks and streptozotocin [STZ]; 40 mg/kg body weight {BW}) in groups B, C, D, E, and F were also administered distilled water (DW), metformin (100 mg/kg BW), 11.2, 22.3, and 44.6 mg/kg BW of AETPL, respectively, whilst non-diabetic rats in Group A received DW only (Sham Control, SC) for 14 days. The T2DM-related parameters were then evaluated.</div></div><div><h3>Results</h3><div>The fructose-fed streptozotocin-(FSTZ) treatment related significant (p < 0.05) increases in FBS, HbA1c, fructosamine, HOMA-IR, G6P, GP, TC, TG, LDL-C, urea, bilirubin, hepatic and pancreatic MDA levels; decreases in BW, serum insulin, creatinine, albumin, HOMA-β, glycogen, G6PD, HK, HDL-C, hepatic and pancreatic SOD, GPX, RG, catalase, Hb, PCV, MCH, MCHC, MCV, RBC, WBC, differentials and the destruction of the pancreatic <u>β</u>-cells, hepatocyte degeneration, and central hepatic vein congestion were reversed by AETPL, to values that compared well with SC in most cases. In the IpGGT model, the intraperitoneally administered AETPL reduced the blood glucose and elevated the plasma insulin levels. The AETPL at 44.6 mg/kg BW exhibited the most pronounced effects.</div></div><div><h3>Conclusion</h3><div>AETPL (44.6 mg/kg BW) restored T2DM-glycemic control and associated biochemical changes via up-regulation of insulin, carbohydrate metabolizing enzymes and restoration of pancreatic and hepatic histoarchitecture.</div></div>","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 509-521"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141849539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2024.08.003
Qihua Yu , Jiagu Ke , Baolin Xie , Ning Li , Miaomiao Zhang , Lipeng Tang , Xiong Li , Chuanjian Lu , Dinghong Wu
Background
Psoriasis is a chronic skin disease that causes inflammation over time due to immune cell-mediated inflammation, oxidative stress, and lipid mediator imbalance. This study was to investigate the impact of Yinxieling (YXL), a reliable Chinese medicine for the treatment of psoriasis vulgaris, on the redox balance and lipid mediators in mice with IMQ-induced psoriasis.
Methods
Daily application of aqueous extract of YXL on IMQ-induced psoriasis-like mice, the efficacy and mechanism of YXL were evaluated by appearance symptoms, oxidative stress indicators, immune balance, and lipid metabolism indicators.
Results
The results demonstrated that YXL significantly enhanced therapeutic efficacy in a psoriasis mouse model, markedly improving the PASl scores and cutaneous inflammation. Upon YXL treatment, lipid peroxidation levels were significantly reduced, while antioxidant levels correspondingly increased. Additionally, YXL modulated the metabolic enzymes associated with 2-AG, which led to a decrease in CB1 receptor expression and an increase in CB2 receptor expression. In terms of immune modulation, YXL treatment promoted the regulation of T cell populations by down-regulating Th1, Th17, and γδT cells, while up-regulating Th2 and Treg cells, thereby facilitating the formation of an anti-inflammatory state. Further analysis indicated that these regulatory effects were closely associated with the down-regulation of NF-kB expression and the up-regulation of Nrf2 expression.
Conclusion
In conclusion, YXL reduces mice dermatitis by inhibiting oxidative stress, elevating endocannabinoid levels and balancing T cell populations in IMQ-induced psoriasis through the NF-κB and Nrf2 signaling pathways. Our results suggest its potential as a therapeutic option for psoriasis by targeting multiple pathways involved in the disease's development.
{"title":"Yinxieling attenuates psoriasis in mice by regulating oxidative stress and lipid mediators to correct immune cell disorder through the NF-κB/Nrf2 signaling pathways","authors":"Qihua Yu , Jiagu Ke , Baolin Xie , Ning Li , Miaomiao Zhang , Lipeng Tang , Xiong Li , Chuanjian Lu , Dinghong Wu","doi":"10.1016/j.jtcme.2024.08.003","DOIUrl":"10.1016/j.jtcme.2024.08.003","url":null,"abstract":"<div><h3>Background</h3><div>Psoriasis is a chronic skin disease that causes inflammation over time due to immune cell-mediated inflammation, oxidative stress, and lipid mediator imbalance. This study was to investigate the impact of Yinxieling (YXL), a reliable Chinese medicine for the treatment of psoriasis vulgaris, on the redox balance and lipid mediators in mice with IMQ-induced psoriasis.</div></div><div><h3>Methods</h3><div>Daily application of aqueous extract of YXL on IMQ-induced psoriasis-like mice, the efficacy and mechanism of YXL were evaluated by appearance symptoms, oxidative stress indicators, immune balance, and lipid metabolism indicators.</div></div><div><h3>Results</h3><div>The results demonstrated that YXL significantly enhanced therapeutic efficacy in a psoriasis mouse model, markedly improving the PASl scores and cutaneous inflammation. Upon YXL treatment, lipid peroxidation levels were significantly reduced, while antioxidant levels correspondingly increased. Additionally, YXL modulated the metabolic enzymes associated with 2-AG, which led to a decrease in CB1 receptor expression and an increase in CB2 receptor expression. In terms of immune modulation, YXL treatment promoted the regulation of T cell populations by down-regulating Th1, Th17, and γδT cells, while up-regulating Th2 and Treg cells, thereby facilitating the formation of an anti-inflammatory state. Further analysis indicated that these regulatory effects were closely associated with the down-regulation of NF-kB expression and the up-regulation of Nrf2 expression.</div></div><div><h3>Conclusion</h3><div>In conclusion, YXL reduces mice dermatitis by inhibiting oxidative stress, elevating endocannabinoid levels and balancing T cell populations in IMQ-induced psoriasis through the NF-κB and Nrf2 signaling pathways. Our results suggest its potential as a therapeutic option for psoriasis by targeting multiple pathways involved in the disease's development.</div></div>","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 548-558"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2024.07.005
Guiting Zhou , Chenxi Wang , Zhichao Lin , Liwen Lin , Ruochen Zhu , Shushu Wang , Jiongbo Xu , Yuxin Xie , Yuling Zhang , Danling Cheng , Chun Zhou , Juan Lin , Haibiao Guo , Min Liu , Chuanjin Luo
Background and aim
Nao-Xin-Qing (NXQ) tablets are standardized proprietary herbal products containing an extract of Chinese persimmon leaves (Diospyros kaki L.f., World Checklist) and other natural ingredients. NXQ has also been indicated for atherosclerosis (AS), but the mechanisms of its antiatherosclerotic activity are unclear. In this study, its mechanisms were investigated by using preclinical models, and provide evidence for its potential application against cardiovascular disorders.
Experimental procedure
In vivo, the apolipoprotein E-deficient (ApoE−/−) mice were fed with a high-fat diet to induce AS. And the mice were treated with different concentrations of NXQ and Lipitor for 12 weeks. After the intervention, serum lipid levels and serum inflammatory factor levels were measured. The pathological changes in the aorta were observed by Oil-red-O staining and Hematoxylin and Eosin (HE) staining. Additionally, we investigated macrophage polarization both in vivo and in vitro. Using the NXQ fingerprint, we conducted network pharmacological analysis to predict and explore its antiatherosclerotic mechanism, which was validated in AS mice and LPS-induced macrophages.
Results
In our study, we found that NXQ significantly reduced atherosclerotic plaques in the aortic root and aorta and decreased serum lipid levels in HFD-fed ApoE−/− mice. Meanwhile, NXQ promoted M2 macrophage polarization, which is regulated by the AMPK-α/SIRT1/PPAR-γ axis. Importantly, suppressing AMPK-α eliminated the effect of NXQ on macrophages.
Conclusion
NXQ exerted a preventive effect on the development and progression of AS by promoting M2 macrophage polarization through modulation of the AMPK-α/SIRT1/PPAR-γ axis.
脑心清（NXQ）片是一种标准化的专利草药产品，含有柿叶提取物（Diospyros kaki L.f., World Checklist）和其他天然成分。NXQ也被用于动脉粥样硬化（AS），但其抗动脉粥样硬化活性的机制尚不清楚。本研究通过临床前模型研究其作用机制，为其在心血管疾病治疗中的潜在应用提供依据。实验方法：在体内，给载脂蛋白e缺乏（ApoE−/−）小鼠喂食高脂饲料以诱导AS。用不同浓度的NXQ和立普妥治疗小鼠12周。干预后，测量血脂水平和血清炎症因子水平。采用油红o染色、苏木精伊红（HE）染色观察主动脉的病理变化。此外，我们还研究了巨噬细胞在体内和体外的极化。我们利用NXQ指纹图谱进行网络药理分析，预测和探索其抗动脉粥样硬化机制，并在AS小鼠和lps诱导的巨噬细胞中得到验证。结果在我们的研究中，我们发现NXQ显著减少了hfd喂养的ApoE - / -小鼠主动脉根部和主动脉的动脉粥样硬化斑块，降低了血清脂质水平。同时，NXQ促进M2巨噬细胞极化，这一过程受AMPK-α/SIRT1/PPAR-γ轴调控。重要的是，抑制AMPK-α可消除NXQ对巨噬细胞的作用。结论nxq通过调节AMPK-α/SIRT1/PPAR-γ轴促进M2巨噬细胞极化，对AS的发生发展具有预防作用。
{"title":"Nao-Xin-Qing tablet inhibits macrophage inflammatory response in atherosclerosis via AMPK-α/SIRT1/PPAR-γ pathway","authors":"Guiting Zhou , Chenxi Wang , Zhichao Lin , Liwen Lin , Ruochen Zhu , Shushu Wang , Jiongbo Xu , Yuxin Xie , Yuling Zhang , Danling Cheng , Chun Zhou , Juan Lin , Haibiao Guo , Min Liu , Chuanjin Luo","doi":"10.1016/j.jtcme.2024.07.005","DOIUrl":"10.1016/j.jtcme.2024.07.005","url":null,"abstract":"<div><h3>Background and aim</h3><div>Nao-Xin-Qing (NXQ) tablets are standardized proprietary herbal products containing an extract of Chinese persimmon leaves (<em>Diospyros kaki</em> L.f., World Checklist) and other natural ingredients. NXQ has also been indicated for atherosclerosis (AS), but the mechanisms of its antiatherosclerotic activity are unclear. In this study, its mechanisms were investigated by using preclinical models, and provide evidence for its potential application against cardiovascular disorders.</div></div><div><h3>Experimental procedure</h3><div>In vivo, the apolipoprotein E-deficient (ApoE<sup>−/−</sup>) mice were fed with a high-fat diet to induce AS. And the mice were treated with different concentrations of NXQ and Lipitor for 12 weeks. After the intervention, serum lipid levels and serum inflammatory factor levels were measured. The pathological changes in the aorta were observed by Oil-red-O staining and Hematoxylin and Eosin (HE) staining. Additionally, we investigated macrophage polarization both in vivo and in vitro. Using the NXQ fingerprint, we conducted network pharmacological analysis to predict and explore its antiatherosclerotic mechanism, which was validated in AS mice and LPS-induced macrophages.</div></div><div><h3>Results</h3><div>In our study, we found that NXQ significantly reduced atherosclerotic plaques in the aortic root and aorta and decreased serum lipid levels in HFD-fed ApoE<sup>−/−</sup> mice. Meanwhile, NXQ promoted M2 macrophage polarization, which is regulated by the AMPK-α/SIRT1/PPAR-γ axis. Importantly, suppressing AMPK-α eliminated the effect of NXQ on macrophages.</div></div><div><h3>Conclusion</h3><div>NXQ exerted a preventive effect on the development and progression of AS by promoting M2 macrophage polarization through modulation of the AMPK-α/SIRT1/PPAR-γ axis.</div></div>","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 536-547"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141848000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2024.06.006
Khalid Imtiyaz, Mohsin Shafi, Khalid Umar Fakhri, Laraib Uroog, Bushra Zeya, Syed Tauqeer Anwer, M Moshahid Alam Rizvi
Cancer poses a significant global health challenge, contributing to substantial mortality rates and driving the urgent need for exploration into bioactive compounds with potent anticancer properties. Polydatin (PD), a stilbenoid compound abundant in various fruits and vegetables, has emerged as a promising candidate in cancer research. Renowned in traditional Chinese medicine for its multifaceted biological activities encompassing antioxidant, anti-inflammatory, anticancer, hepatoprotective, neuroprotective, and immunostimulatory effects, PD stands out as a versatile therapeutic agent. This review paper meticulously compiles the diverse anticancer attributes of polydatin across a spectrum of cancer types, elucidating its impact on pivotal cancer hallmarks such as proliferation, migration, metastasis, apoptosis, modulation of the tumour microenvironment, autophagy, and more. Furthermore, the review intricately explores the intricate pathways influenced by polydatin within cancer cells, unveiling its mechanisms of action and identifying potential therapeutic targets. By providing a comprehensive analysis of how polydatin affects various facets of cancer progression and addresses treatment resistance, this paper aims to enhance our understanding of its pivotal role in cancer therapy. Moreover, the synergistic potential of polydatin in combination with other drugs is investigated to underscore its amplified efficacy in combating cancer through innovative mechanism-based strategies. The synthesis of these insights underscores polydatin's significance as a valuable component in the advancement of novel approaches to cancer prevention and treatment.
Goals
This review aims to comprehensively compile and analyze the diverse anticancer attributes of polydatin (PD) across various cancer types, elucidating its impact on pivotal cancer hallmarks such as proliferation, migration, metastasis, apoptosis, and modulation of the tumour microenvironment. Additionally, it explores the intricate pathways influenced by polydatin within cancer cells, unveiling its mechanisms of action and identifying potential therapeutic targets. Moreover, the review investigates polydatin's potential synergistic effects with other anticancer drugs, while also examining its therapeutic and preventive effects against various cancers.
Methods
A systematic review of scientific literature, comprising research articles, clinical trials, and reviews, was conducted to analyze polydatin's anticancer properties. Reputable databases like PubMed, ScienceDirect, and Google Scholar were searched, and selected studies were critically evaluated to extract essential insights into polydatin's mechanisms of action and its interactions with other anticancer drugs, utilizing keywords targeting specific cancer types such as colorectal, oral, breast, and cervical cancer.
{"title":"Polydatin: A natural compound with multifaceted anticancer properties","authors":"Khalid Imtiyaz, Mohsin Shafi, Khalid Umar Fakhri, Laraib Uroog, Bushra Zeya, Syed Tauqeer Anwer, M Moshahid Alam Rizvi","doi":"10.1016/j.jtcme.2024.06.006","DOIUrl":"10.1016/j.jtcme.2024.06.006","url":null,"abstract":"<div><div>Cancer poses a significant global health challenge, contributing to substantial mortality rates and driving the urgent need for exploration into bioactive compounds with potent anticancer properties. Polydatin (PD), a stilbenoid compound abundant in various fruits and vegetables, has emerged as a promising candidate in cancer research. Renowned in traditional Chinese medicine for its multifaceted biological activities encompassing antioxidant, anti-inflammatory, anticancer, hepatoprotective, neuroprotective, and immunostimulatory effects, PD stands out as a versatile therapeutic agent. This review paper meticulously compiles the diverse anticancer attributes of polydatin across a spectrum of cancer types, elucidating its impact on pivotal cancer hallmarks such as proliferation, migration, metastasis, apoptosis, modulation of the tumour microenvironment, autophagy, and more. Furthermore, the review intricately explores the intricate pathways influenced by polydatin within cancer cells, unveiling its mechanisms of action and identifying potential therapeutic targets. By providing a comprehensive analysis of how polydatin affects various facets of cancer progression and addresses treatment resistance, this paper aims to enhance our understanding of its pivotal role in cancer therapy. Moreover, the synergistic potential of polydatin in combination with other drugs is investigated to underscore its amplified efficacy in combating cancer through innovative mechanism-based strategies. The synthesis of these insights underscores polydatin's significance as a valuable component in the advancement of novel approaches to cancer prevention and treatment.</div></div><div><h3>Goals</h3><div>This review aims to comprehensively compile and analyze the diverse anticancer attributes of polydatin (PD) across various cancer types, elucidating its impact on pivotal cancer hallmarks such as proliferation, migration, metastasis, apoptosis, and modulation of the tumour microenvironment. Additionally, it explores the intricate pathways influenced by polydatin within cancer cells, unveiling its mechanisms of action and identifying potential therapeutic targets. Moreover, the review investigates polydatin's potential synergistic effects with other anticancer drugs, while also examining its therapeutic and preventive effects against various cancers.</div></div><div><h3>Methods</h3><div>A systematic review of scientific literature, comprising research articles, clinical trials, and reviews, was conducted to analyze polydatin's anticancer properties. Reputable databases like PubMed, ScienceDirect, and Google Scholar were searched, and selected studies were critically evaluated to extract essential insights into polydatin's mechanisms of action and its interactions with other anticancer drugs, utilizing keywords targeting specific cancer types such as colorectal, oral, breast, and cervical cancer.</div></div><div><h3>Findings</h3><div>The review and additional online","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 447-466"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2024.06.008
Vaishnavi Rathi, Sarada S.K. Sagi
The objective of the present study is to decipher the role of NF-κB and its associated downstream genes involved in causing inflammation in kidneys of rats under acute hypobaric hypoxia exposure. The study also aims at finding out the efficacy of quercetin in comparison with dexamethasone in prevention of hypobaric hypoxia induced renal inflammation. Sprague Dawley (SD) rats (n = 6) were preconditioned with 50 mg/Kg BW of quercetin, 1 h prior to hypobaric hypoxia exposure (12 h). The results revealed a significant increase in reactive oxygen species (ROS) generation and malondialdehyde (MDA) (p < 0.001) levels along with down regulation of GPx and SOD levels in kidney tissue of hypobaric hypoxia exposed rats as compared to control. However, ROS production and MDA levels in kidney tissues were reduced significantly (p < 0.001) with enhanced antioxidant enzyme levels (GPx and SOD) in rats fed with quercetin as compared to hypobaric hypoxia exposed control (p < 0.001). Protein expression analysis through western blotting and EMSA performed in nuclear extracts of kidneys, exhibited a significant upregulation of NF-κB under hypobaric hypoxic stress as compared to control. Whereas pretreatment with quercetin aids in downregulation of NF-κB expression in kidneys of rats as compared to the hypobaric hypoxia exposed group. Further, quercetin prophylaxis significantly reduced the expression of pro-inflammatory cytokines (TNF-α, IL-2 and IL-6), increased the anti-inflammatory cytokines (IL-10, IL-4 and TGF-β) along with reduced expression of cell adhesion molecules (ICAM-1, VCAM-1, E-selectin and P-selectin) in kidneys of rats under hypobaric hypoxia as compared to hypobaric hypoxia control. However, pre-treatment with dexamethasone was not as effective as quercetin, in controlling the renal inflammation. Furthermore, improved hematological parameters such as WBC, RBC, and platelet count indicated that quercetin is a well-functioning effective molecule under hypobaric hypoxic exposure. The histopathological and TEM findings, manifested the structural changes in tubular arrangements in kidneys of rats, and these changes were found to be modified by quercetin prophylaxis under hypobaric hypoxic stress. Hence, the present study indicates that, quercetin can be considered as a potential phytochemical flavonoid moiety in preventing the acute renal inflammation under hypobaric hypoxia.
{"title":"Mitigation of hypobaric hypoxia induced renal inflammatory alterations by quercetin prophylaxis","authors":"Vaishnavi Rathi, Sarada S.K. Sagi","doi":"10.1016/j.jtcme.2024.06.008","DOIUrl":"10.1016/j.jtcme.2024.06.008","url":null,"abstract":"<div><div>The objective of the present study is to decipher the role of NF-κB and its associated downstream genes involved in causing inflammation in kidneys of rats under acute hypobaric hypoxia exposure. The study also aims at finding out the efficacy of quercetin in comparison with dexamethasone in prevention of hypobaric hypoxia induced renal inflammation. Sprague Dawley (SD) rats (n = 6) were preconditioned with 50 mg/Kg BW of quercetin, 1 h prior to hypobaric hypoxia exposure (12 h). The results revealed a significant increase in reactive oxygen species (ROS) generation and malondialdehyde (MDA) (<em>p</em> < 0.001) levels along with down regulation of GPx and SOD levels in kidney tissue of hypobaric hypoxia exposed rats as compared to control. However, ROS production and MDA levels in kidney tissues were reduced significantly (<em>p</em> < 0.001) with enhanced antioxidant enzyme levels (GPx and SOD) in rats fed with quercetin as compared to hypobaric hypoxia exposed control (<em>p</em> < 0.001). Protein expression analysis through western blotting and EMSA performed in nuclear extracts of kidneys, exhibited a significant upregulation of NF-κB under hypobaric hypoxic stress as compared to control. Whereas pretreatment with quercetin aids in downregulation of NF-κB expression in kidneys of rats as compared to the hypobaric hypoxia exposed group. Further, quercetin prophylaxis significantly reduced the expression of pro-inflammatory cytokines (TNF-α, IL-2 and IL-6), increased the anti-inflammatory cytokines (IL-10, IL-4 and TGF-β) along with reduced expression of cell adhesion molecules (ICAM-1, VCAM-1, E-selectin and P-selectin) in kidneys of rats under hypobaric hypoxia as compared to hypobaric hypoxia control. However, pre-treatment with dexamethasone was not as effective as quercetin, in controlling the renal inflammation. Furthermore, improved hematological parameters such as WBC, RBC, and platelet count indicated that quercetin is a well-functioning effective molecule under hypobaric hypoxic exposure. The histopathological and TEM findings, manifested the structural changes in tubular arrangements in kidneys of rats, and these changes were found to be modified by quercetin prophylaxis under hypobaric hypoxic stress. Hence, the present study indicates that, quercetin can be considered as a potential phytochemical flavonoid moiety in preventing the acute renal inflammation under hypobaric hypoxia.</div></div>","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 482-494"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2024.07.007
Xiao-jie Bai , Jun-tao Hao , Qi-long Feng , Chen-meng Guo , Min Pang , Jia Li , Jin Wang , Jian-feng Xing
Background and aim
Curcumin has shown significant cardiovascular protective effects. However, the low bioavailability limits its practical application. As a natural bioenhancer, piperine is expected to increase the bioavailability of curcumin, and then, enhance its beneficial effects. Meanwhile, glucagon-like peptide-1 receptor (GLP-1R) signaling has been confirmed to be involved in the regulation of cardiovascular events. Herein, this study aimed to investigate whether piperine could enhance the beneficial effects of curcumin in pressure-overload rats and whether GLP-1/GLP-1R signaling is involved in their action mechanism.
Methods and results
Male Sprague-Dawley (SD) adult rats were subjected to abdominal aortic constriction (AAC) surgery to 16 weeks, which elevated blood pressure and induced cardiac hypertrophy. Curcumin (100 mg/kg/day) or/and piperine (20 mg/kg/day) were orally given for 4 weeks from the 17th week after AAC surgery. Curcumin alone treatment significantly lowered blood pressure, ameliorated cardiovascular remodeling, improved left ventricular performance and endothelium-dependent vascular relaxation. Accompanied by these results, GLP-1R expression in the myocardium was up-regulated. Piperine alone also exhibited a certain positive inotropic cardiac activity, but the effect was less significant. The combination of curcumin and piperine didn't show enhanced cardiovascular protective effects relative to curcumin, along with decreased fasting serum GLP-1 level and GLP-1R expression in the myocardium.
Conclusion
Curcumin exerts cardiovascular protective effects in pressure-overload rats by upregulating GLP-1R, and inhibiting of GLP-1/GLP-1R signaling pathway may be related to the limited beneficial effects of combination of curcumin and piperine. This study provides a new thinking that oral administration of some spices may affect cardiovascular function by modulating the GLP-1/GLP-1R system in a mode of gut-heart axis regulation.
{"title":"Curcumin alone not combined with piperine exerts cardioprotective effects in pressure-overload rats by increasing glucagon-like peptide-1 receptor signaling and additional properties","authors":"Xiao-jie Bai , Jun-tao Hao , Qi-long Feng , Chen-meng Guo , Min Pang , Jia Li , Jin Wang , Jian-feng Xing","doi":"10.1016/j.jtcme.2024.07.007","DOIUrl":"10.1016/j.jtcme.2024.07.007","url":null,"abstract":"<div><h3>Background and aim</h3><div>Curcumin has shown significant cardiovascular protective effects. However, the low bioavailability limits its practical application. As a natural bioenhancer, piperine is expected to increase the bioavailability of curcumin, and then, enhance its beneficial effects. Meanwhile, glucagon-like peptide-1 receptor (GLP-1R) signaling has been confirmed to be involved in the regulation of cardiovascular events. Herein, this study aimed to investigate whether piperine could enhance the beneficial effects of curcumin in pressure-overload rats and whether GLP-1/GLP-1R signaling is involved in their action mechanism.</div></div><div><h3>Methods and results</h3><div>Male Sprague-Dawley (SD) adult rats were subjected to abdominal aortic constriction (AAC) surgery to 16 weeks, which elevated blood pressure and induced cardiac hypertrophy. Curcumin (100 mg/kg/day) or/and piperine (20 mg/kg/day) were orally given for 4 weeks from the 17th week after AAC surgery. Curcumin alone treatment significantly lowered blood pressure, ameliorated cardiovascular remodeling, improved left ventricular performance and endothelium-dependent vascular relaxation. Accompanied by these results, GLP-1R expression in the myocardium was up-regulated. Piperine alone also exhibited a certain positive inotropic cardiac activity, but the effect was less significant. The combination of curcumin and piperine didn't show enhanced cardiovascular protective effects relative to curcumin, along with decreased fasting serum GLP-1 level and GLP-1R expression in the myocardium.</div></div><div><h3>Conclusion</h3><div>Curcumin exerts cardiovascular protective effects in pressure-overload rats by upregulating GLP-1R, and inhibiting of GLP-1/GLP-1R signaling pathway may be related to the limited beneficial effects of combination of curcumin and piperine. This study provides a new thinking that oral administration of some spices may affect cardiovascular function by modulating the GLP-1/GLP-1R system in a mode of gut-heart axis regulation.</div></div>","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 522-535"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141848008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2024.07.002
Shiqi Li , Yuanping Wang , Xulan Cui , Xiaoyu Tian , Ziwei Huang , Rong Zhang , Yuanyuan Cheng , Zhongqiu Liu , Dawei Wang
Background
Water retention is one of the important factors in the development and exacerbation of chronic heart failure (CHF). Xinbao Pill (XBP) is widely used as an adjuvant therapy for CHF. However, the therapeutic effect of XBP on water retention in CHF remains unclear.
Purpose
Our research was aimed to investigate the effect and mechanism of XBP on water retention in CHF.
Methods
Male Sprague-Dawley (SD) rats underwent left anterior descending (LAD) artery ligation to establish the CHF model and were subsequently administrated with different doses of XBP or Qili Qiangxin (QLQX). Cardiac functions were assessed using M-mode echocardiography. Cardiac remodeling and myocardial fibrosis were observed using HE and Masson staining. Additionally, the expression of the CaSR/AQP2 signaling pathway in the renal was detected using western blotting analysis, quantitative PCR analysis, immunofluorescence staining, immunohistochemistry, and co-immunoprecipitation assays. Furthermore, CaSR inhibitor NPS2143 was used to confirm the role of CaSR on the effect of XBP for water retention.
Results
In the LAD-induced CHF rat model, XBP improved EF (ejection fraction) and LVFS (fractional shortening), and alleviated cardiac fibrosis. Importantly, XBP significantly increased the 24-h urine volume and decreased urinary protein level after CHF. Further mechanism studies showed that XBP treatment could decrease the expression of renal AQP2 at the protein and mRNA levels. Moreover, XBP promoted renal AQP2 ubiquitination by upregulating CaSR and p-p38-MAPK expression. Meanwhile, XBP suppressed the expression of p-CREB to inhibit the mRNA expression of AQP2 in the renal tissue. However, NPS2143 blocked the beneficial effects of XBP on cardiac function and water retention, even stopped the inhibitory effect on AQP2 expression by XBP.
Conclusion
Our study revealed that XBP improved water retention against CHF via promoting CaSR/p38-MAPK-mediated AQP2 ubiquitination and regulating CaSR/CREB-mediated AQP2 transcription.
{"title":"Xinbao pill attenuated water retention by regulating the CaSR/AQP2 pathway in LAD-induced chronic heart failure rats","authors":"Shiqi Li , Yuanping Wang , Xulan Cui , Xiaoyu Tian , Ziwei Huang , Rong Zhang , Yuanyuan Cheng , Zhongqiu Liu , Dawei Wang","doi":"10.1016/j.jtcme.2024.07.002","DOIUrl":"10.1016/j.jtcme.2024.07.002","url":null,"abstract":"<div><h3>Background</h3><div>Water retention is one of the important factors in the development and exacerbation of chronic heart failure (CHF). Xinbao Pill (XBP) is widely used as an adjuvant therapy for CHF. However, the therapeutic effect of XBP on water retention in CHF remains unclear.</div></div><div><h3>Purpose</h3><div>Our research was aimed to investigate the effect and mechanism of XBP on water retention in CHF.</div></div><div><h3>Methods</h3><div>Male Sprague-Dawley (SD) rats underwent left anterior descending (LAD) artery ligation to establish the CHF model and were subsequently administrated with different doses of XBP or Qili Qiangxin (QLQX). Cardiac functions were assessed using M-mode echocardiography. Cardiac remodeling and myocardial fibrosis were observed using HE and Masson staining. Additionally, the expression of the CaSR/AQP2 signaling pathway in the renal was detected using western blotting analysis, quantitative PCR analysis, immunofluorescence staining, immunohistochemistry, and co-immunoprecipitation assays. Furthermore, CaSR inhibitor NPS2143 was used to confirm the role of CaSR on the effect of XBP for water retention.</div></div><div><h3>Results</h3><div>In the LAD-induced CHF rat model, XBP improved EF (ejection fraction) and LVFS (fractional shortening), and alleviated cardiac fibrosis. Importantly, XBP significantly increased the 24-h urine volume and decreased urinary protein level after CHF. Further mechanism studies showed that XBP treatment could decrease the expression of renal AQP2 at the protein and mRNA levels. Moreover, XBP promoted renal AQP2 ubiquitination by upregulating CaSR and p-p38-MAPK expression. Meanwhile, XBP suppressed the expression of p-CREB to inhibit the mRNA expression of AQP2 in the renal tissue. However, NPS2143 blocked the beneficial effects of XBP on cardiac function and water retention, even stopped the inhibitory effect on AQP2 expression by XBP.</div></div><div><h3>Conclusion</h3><div>Our study revealed that XBP improved water retention against CHF via promoting CaSR/p38-MAPK-mediated AQP2 ubiquitination and regulating CaSR/CREB-mediated AQP2 transcription.</div></div>","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 495-508"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141704016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2024.11.011
Yong Wen , Yu Zhan , Li-juan Du , Jun Li , Xu-long Shen , Bin He , Tai-yu Chen , Xue-gui Tang
Aurantii fructus immaturus flavonoid (AFIF) is the main constituent of Aurantii fructus immaturus (Rutaceae) (AFI), and is effective against constipation. This study explores the mechanism of AFIF against antibiotics-induced constipation (AC) in mice. Forty six-week-old female C57BL/6 mice were randomly divided into 4 groups (n = 10): control, control + AFIF, model, and model + AFIF groups. The AC model was established by antibiotics mixture for 8 days. Mice were gavaged daily with AFIF (0.1 mL/10 g, 3 g/mL) for 2 weeks. Hematoxylin and eosin (H&E) staining and periodic acid-Schiff (PAS) staining were used for histological analysis. The colonic microbiota was analyzed by 16sRNA sequencing. Transcriptome sequencing was used to detect miRNA and mRNA expression profiles. The results showed that AFIF treatment improved constipation in AC mice: increased fecal number, fecal wet weight, fecal water content, and intestinal propulsion rate; decreased average weight of individual feces. AFIF improved the colonic pathological injury and increased acetylcholine (ACH), gastrin (GAS), motilin (MTL), substance P (SP), and vasoactive intestinal peptide (VIP) levels. Moreover, AFIF might improve AC by regulating colonic microbiota and a “miRNA-mRNA” regulatory network related to cell junction and neuroactive function. This study also found the colonic microbiota at the genus level was connected to the expressions and target mRNA expressions (including Ccdc85b, Dlgap2, Elavl4, and Shisa6) of mmu-miR-5100 and mmu-miR-18b-5p. In conclusions, AFIF could improve AC via regulating colonic microbiota and a “miRNA-mRNA” regulatory network, which provide a theoretical basis for expanding its clinical application.
{"title":"Aurantii fructus immaturus (Rutaceae) flavonoid ameliorated constipation by regulating colonic microbiota and miRNA/mRNA network","authors":"Yong Wen , Yu Zhan , Li-juan Du , Jun Li , Xu-long Shen , Bin He , Tai-yu Chen , Xue-gui Tang","doi":"10.1016/j.jtcme.2024.11.011","DOIUrl":"10.1016/j.jtcme.2024.11.011","url":null,"abstract":"<div><div><em>Aurantii fructus immaturus</em> flavonoid (AFIF) is the main constituent of <em>Aurantii fructus immaturus</em> (Rutaceae) (AFI), and is effective against constipation. This study explores the mechanism of AFIF against antibiotics-induced constipation (AC) in mice. Forty six-week-old female C57BL/6 mice were randomly divided into 4 groups (<em>n</em> = 10): control, control + AFIF, model, and model + AFIF groups. The AC model was established by antibiotics mixture for 8 days. Mice were gavaged daily with AFIF (0.1 mL/10 g, 3 g/mL) for 2 weeks. Hematoxylin and eosin (H&E) staining and periodic acid-Schiff (PAS) staining were used for histological analysis. The colonic microbiota was analyzed by 16sRNA sequencing. Transcriptome sequencing was used to detect miRNA and mRNA expression profiles. The results showed that AFIF treatment improved constipation in AC mice: increased fecal number, fecal wet weight, fecal water content, and intestinal propulsion rate; decreased average weight of individual feces. AFIF improved the colonic pathological injury and increased acetylcholine (ACH), gastrin (GAS), motilin (MTL), substance P (SP), and vasoactive intestinal peptide (VIP) levels. Moreover, AFIF might improve AC by regulating colonic microbiota and a “miRNA-mRNA” regulatory network related to cell junction and neuroactive function. This study also found the colonic microbiota at the genus level was connected to the expressions and target mRNA expressions (including Ccdc85b, Dlgap2, Elavl4, and Shisa6) of mmu-miR-5100 and mmu-miR-18b-5p. In conclusions, AFIF could improve AC via regulating colonic microbiota and a “miRNA-mRNA” regulatory network, which provide a theoretical basis for expanding its clinical application.</div></div>","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 559-572"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.jtcme.2024.06.007
Deepa Mandlik, Rutuja Patil, S. Arulmozhi, Satish Mandlik
Background and aim
Kerala Ayurveda Ostoact Tablet (OAT) is a traditional Ayurvedic preparation that might use for the management of joint pain, bone pain and arthritis. The goal of present research was to evaluate the activity of OAT in improving postmenopausal osteoporosis (PMO) in ovariectomized (OVX) rats.
Experimental procedures
Female rats were ovariectomized bilaterally and distributed into 6 groups (n = 8) as Sham control (SC), Ovariectomy control (OVX), OVX with OAT (50 mg/kg, p.o.), OVX with OAT (100 mg/kg, p.o.) and OVX with OAT (150 mg/kg, p.o.) and Standard group (17β-estradiol, 30 μg/kg, s.c.). SC group rats went through a sham operation procedure. The animals were treated with an oral dose of OAT (50, 100 and 150 mg/kg) for 90 days. Body weight, tail skin temperature (TST) Serum hormones, bone turnover parameters, proinflammatory cytokines, bone physical parameters, histopathological analysis (uterus, vagina, and femur) and microcomputed tomography of the femur were measured on the 90th day of treatment. A new high performance thin layer chromatography (HPTLC) process has been established for the standardization of OAT.
Results and conclusion
OVX rats treated with OAT exhibited a significant decrease in TST, improved serum hormonal and lipid profile, bone turnover markers and pro-inflammatory cytokines, bone physical properties, increased bone density, and enhanced cytological and histological alterations with significant improvement in rat's body weight. In addition, OAT administration enhanced the weakening of trabecular bone microarchitecture triggered by OVX confirmed by microcomputed tomography (micro-CT). These findings imply that OAT may help treat osteoporosis in women brought on by menopause.
{"title":"Kerala Ayurveda Ostoact Tablet treats osteoporosis in ovariectomized rat model via regulating RANKL/OPG pathway","authors":"Deepa Mandlik, Rutuja Patil, S. Arulmozhi, Satish Mandlik","doi":"10.1016/j.jtcme.2024.06.007","DOIUrl":"10.1016/j.jtcme.2024.06.007","url":null,"abstract":"<div><h3>Background and aim</h3><div>Kerala Ayurveda Ostoact Tablet (OAT) is a traditional Ayurvedic preparation that might use for the management of joint pain, bone pain and arthritis. The goal of present research was to evaluate the activity of OAT in improving postmenopausal osteoporosis (PMO) in ovariectomized (OVX) rats.</div></div><div><h3>Experimental procedures</h3><div>Female rats were ovariectomized bilaterally and distributed into 6 groups (n = 8) as Sham control (SC), Ovariectomy control (OVX), OVX with OAT (50 mg/kg, p.o.), OVX with OAT (100 mg/kg, p.o.) and OVX with OAT (150 mg/kg, p.o.) and Standard group (17β-estradiol, 30 μg/kg, s.c.). SC group rats went through a sham operation procedure. The animals were treated with an oral dose of OAT (50, 100 and 150 mg/kg) for 90 days. Body weight, tail skin temperature (TST) Serum hormones, bone turnover parameters, proinflammatory cytokines, bone physical parameters, histopathological analysis (uterus, vagina, and femur) and microcomputed tomography of the femur were measured on the 90th day of treatment. A new high performance thin layer chromatography (HPTLC) process has been established for the standardization of OAT.</div></div><div><h3>Results and conclusion</h3><div>OVX rats treated with OAT exhibited a significant decrease in TST, improved serum hormonal and lipid profile, bone turnover markers and pro-inflammatory cytokines, bone physical properties, increased bone density, and enhanced cytological and histological alterations with significant improvement in rat's body weight. In addition, OAT administration enhanced the weakening of trabecular bone microarchitecture triggered by OVX confirmed by microcomputed tomography (micro-CT). These findings imply that OAT may help treat osteoporosis in women brought on by menopause.</div></div>","PeriodicalId":17449,"journal":{"name":"Journal of Traditional and Complementary Medicine","volume":"15 5","pages":"Pages 467-481"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141407304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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