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Integrating serum pharmacochemistry, network pharmacology, and metabolomics to elucidate the detoxification and effect-adjusting mechanism of Chebulae Fructus-processing on Mongolian medicine Euphorbia pekinensis
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-05 DOI: 10.1016/j.jep.2025.119582
Bingbing Liu , Min Zeng , Wenqingqing Kang , Shu Li , Xinzhi Wang , Hongli Yu , Hao Wu

Ethnopharmacological relevance

Euphorbia pekinensis Radix (EP) is a traditional medicinal plant widely used in Mongolian and Chinese medicine for its potent therapeutic properties in treating edema, ascites, and various inflammatory conditions. However, EP has toxicity, which can cause swelling and congestion of the gastrointestinal mucosa. Chebulae Fructus is a unique processing method in Mongolian medicine that is believed to mitigate EP's toxicity and adjust its effect, though the mechanisms underlying this detoxification remain poorly understood.

Aim of the study

This study employed an integrative approach combining network pharmacology, serum pharmacochemistry, pharmacology, and metabolomics to investigate the intestinal detoxification and synergistic effects of Chebulae Fructus-processed Euphorbia pekinensis (PEP).

Materials and methods

The blood-absorbed components of EP and PEP were identified by UPLC-MS/MS. To evaluate holistic effect of the two medicine, network pharmacology was applied to focus on serum components and identify the key compounds and targets mediating effect in addressing five TCM syndromes, as well as modern medicine symptoms including seven types of cancer and myocardial infarction. In terms of detoxification, non-targeted metabolomics was utilized to analyze significant intestinal metabolites and pathways affected by EP and PEP in normal mice.

Results

A total of 77 and 109 blood-absorbed components were identified from EP and PEP, respectively, including terpenoids, phenolic acids, alkaloids, flavonoids, and tannins. In network pharmacology analysis, key hub genes were identified as therapeutic targets, with PEP exhibiting possibly enhanced effects than EP since it was associated with more targets and diseases in the network. Furthermore, PEP modulated histamine metabolism and arginine biosynthesis pathways, thereby reducing intestinal inflammation.

Conclusion

This study highlights the different anti-cancer and ascites-reducing potential of EP and PEP, emphasizing the detoxification benefits of Chebulae Fructus processing. These findings provide a foundation for the safe and effective therapeutic use of PEP for treating ascites and cancer, while minimizing intestinal toxicity, thereby promoting the safe utilization of medicinal Euphorbiaceae plants.
{"title":"Integrating serum pharmacochemistry, network pharmacology, and metabolomics to elucidate the detoxification and effect-adjusting mechanism of Chebulae Fructus-processing on Mongolian medicine Euphorbia pekinensis","authors":"Bingbing Liu ,&nbsp;Min Zeng ,&nbsp;Wenqingqing Kang ,&nbsp;Shu Li ,&nbsp;Xinzhi Wang ,&nbsp;Hongli Yu ,&nbsp;Hao Wu","doi":"10.1016/j.jep.2025.119582","DOIUrl":"10.1016/j.jep.2025.119582","url":null,"abstract":"<div><h3>Ethnopharmacological relevance</h3><div><em>Euphorbia pekinensis</em> Radix (EP) is a traditional medicinal plant widely used in Mongolian and Chinese medicine for its potent therapeutic properties in treating edema, ascites, and various inflammatory conditions. However, EP has toxicity, which can cause swelling and congestion of the gastrointestinal mucosa. <em>Chebulae Fructus</em> is a unique processing method in Mongolian medicine that is believed to mitigate EP's toxicity and adjust its effect, though the mechanisms underlying this detoxification remain poorly understood.</div></div><div><h3>Aim of the study</h3><div>This study employed an integrative approach combining network pharmacology, serum pharmacochemistry, pharmacology, and metabolomics to investigate the intestinal detoxification and synergistic effects of <em>Chebulae Fructus</em>-processed <em>Euphorbia pekinensis</em> (PEP).</div></div><div><h3>Materials and methods</h3><div>The blood-absorbed components of EP and PEP were identified by UPLC-MS/MS. To evaluate holistic effect of the two medicine, network pharmacology was applied to focus on serum components and identify the key compounds and targets mediating effect in addressing five TCM syndromes, as well as modern medicine symptoms including seven types of cancer and myocardial infarction. In terms of detoxification, non-targeted metabolomics was utilized to analyze significant intestinal metabolites and pathways affected by EP and PEP in normal mice.</div></div><div><h3>Results</h3><div>A total of 77 and 109 blood-absorbed components were identified from EP and PEP, respectively, including terpenoids, phenolic acids, alkaloids, flavonoids, and tannins. In network pharmacology analysis, key hub genes were identified as therapeutic targets, with PEP exhibiting possibly enhanced effects than EP since it was associated with more targets and diseases in the network. Furthermore, PEP modulated histamine metabolism and arginine biosynthesis pathways, thereby reducing intestinal inflammation.</div></div><div><h3>Conclusion</h3><div>This study highlights the different anti-cancer and ascites-reducing potential of EP and PEP, emphasizing the detoxification benefits of <em>Chebulae Fructus</em> processing. These findings provide a foundation for the safe and effective therapeutic use of PEP for treating ascites and cancer, while minimizing intestinal toxicity, thereby promoting the safe utilization of medicinal <em>Euphorbiaceae</em> plants.</div></div>","PeriodicalId":15761,"journal":{"name":"Journal of ethnopharmacology","volume":"345 ","pages":"Article 119582"},"PeriodicalIF":4.8,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143578191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Network pharmacology-based exploration of the mechanism of Wenweishu granule in treating chronic atrophic gastritis with spleen-stomach cold deficiency syndrome
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-05 DOI: 10.1016/j.jep.2025.119591
Jia Zheng , Zhiyong Jiao , Xinyu Yang , Qing Ruan , Yuzhe Huang , Cheng Jin , Shuangying Gui , Zihua Xuan , Xiaoyi Jia

Ethnopharmacological relevance

Wenweishu (WWS) is a traditional Chinese medicine compound formulated for chronic atrophic gastritis (CAG) treatment by warming the stomach and alleviating pain. However, its pharmacological mechanisms remain underexplored.

Aim of the study

This study investigated the therapeutic effects and potential mechanisms of WWS on CAG with spleen-stomach cold deficiency syndrome (SSCDS).

Methods

To achieve this, an SSCDS-CAG rat model and a human gastric mucosal epithelial cells (GES-1) cell model were established using multi-factor modeling and N-Methyl-N′-nitro-N-nitrosoguanidine (MNNG) induction, respectively. WWS's effects on gastric injury were evaluated through pathology, inflammation, serum biomarkers, and apoptosis. Additionally, MNNG's effects on GES-1 cells were analyzed. Network pharmacology, involving protein-protein interaction networks, GO/KEGG enrichment, and molecular docking, was employed to predict WWS's potential targets and mechanisms in SSCDS-CAG. Mechanistic insights were further validated using immunohistochemistry, quantitative reverse transcription polymerase chain reaction, and western blotting.

Results

In vivo results showed that WWS alleviated symptoms in SSCDS-CAG rats, lowering symptom scores and improving gastric histopathology. It modulated serum biomarkers and reduced inflammation and apoptosis in both in vivo and in vitro studies. Network pharmacology results revealed 263 overlapping targets between WWS and SSCDS-CAG, associated with apoptosis, inflammation, and the PI3K/AKT pathway. Molecular docking revealed strong binding affinity between the core target and active WWS components. In SSCDS-CAG rats and GES-1 cells, WWS inhibited PI3K/AKT phosphorylation, increased PTEN expression, and regulated Bcl-2, Bax, and cleaved caspase-3 levels.

Conclusion

WWS reduces inflammation and apoptosis in multi-factor CAG rats and MNNG-induced GES-1 cells by modulating the PTEN/PI3K/AKT signaling pathway and apoptosis-related proteins.
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引用次数: 0
Network pharmacology analysis uncovers the mechanism of Shudihuang-Shanzhuyu herb pair in prevention and treatment of diabetic osteoporosis via PI3K/AKT pathway
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-05 DOI: 10.1016/j.jep.2025.119581
Si-jing Hu , Gao-ce Chen , Fang-yuan Wang , Ying-qi Fang , Si-qi Wang , Zi-le Song , Zi-hui Zhao , Quan-long Zhang , Xiong-yu Meng , Qiao-yan Zhang , Lu-ping Qin

Ethnopharmacological relevance

Diabetic osteoporosis (DOP) is a complication of diabetes characterized by reduced bone mass and increased fracture risk. Shudihuang (Rehmanniae Radix Praeparata, RR) and Shanzhuyu (Corni Fructus, CF) form a classical herb pair known as RR-CF in traditional Chinese medicine (TCM) for nourishing Yin and tonifying the kidney, and have long been used for the treatment of diabetes and OP in TCM clinical practise. However, the potential mechanism underlying the preventive and therapeutic effects of RR-CF on DOP has not been clarified.

Aim of the study

This study aimed to explore the protective effects of RR-CF on bone loss caused by diabetes and elucidate the underlying action mechanism.

Methods

The chemical constituents in RR-CF were detected using UPLC-Q-Exactive-MS. Type 1 diabetes mellitus (T1DM) was induced in rats by injecting streptozotocin, followed by administration of RR-CF extracts for 10 weeks. Bone mineral density, morphometric bone parameters, and serum and urine biochemical markers were analyzed using Micro-CT and ELISA kits. An in vitro osteoblastic injury model was constructed by subjecting MC3T3-E1 cells to high glucose and used to evaluate the effects of the RR-CF on osteoblastic bone formation. The anti-DOP mechanism of RR-CF was explored by network pharmacologic analysis and then verified in osteoblasts damaged by high glucose.

Results

A total of 56 compounds were identified in RR-CF. Treatment with RR-CF extracts improved the bone microstructure and mineral density in the T1DM rats, and decreased the level of urine deoxypyridinoline and serum carboxyl terminal peptide of type I procollagen. The network pharmacology analysis identified cornuside, hydroxygenkwanin, acteoside, catalpol and echinacoside as the potential active components of RR-CF against DOP by interacting with the key node genes such as AKT1, EGFR, TNF, MMP9 and HSP90α. Further GO and KEGG enrichment analysis suggested that the therapeutic effects of RR, CF and RR-CF seemed to be related to the regulation of hormones, inflammation and metabolism, as well as signaling transductions of PI3K-AKT, IL-17, TNF, MAPK and estrogen signaling pathways. RR-CF promoted osteoblast differentiation and bone formation in the MC3T3-E1 cells by regulating PI3K-AKT signaling pathway.

Conclusion

RR-CF herb pair inhibits bone loss caused by high glucose by regulating the PI3K-AKT signaling pathways.
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引用次数: 0
Proteomic analysis reveals that Acalypha australis L. mitigates chronic colitis by modulating the FABP4/PPARγ/NF-κB signaling pathway
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-04 DOI: 10.1016/j.jep.2025.119585
Xiaoyu Quan , Zhiwei Miao , Runxi Han , Rui Deng , Yaqi Cao , Jingshan Tian , Yaping Lu , Guoxiang Wang , Xingjian Yu , Yi Wu , Chen Dai
<div><h3>Ethnopharmacological relevance</h3><div><em>Acalypha australis</em> L. (AAL), a traditional medicinal herb from the Euphorbiaceae family, has been widely used in Chinese medicine for its heat-clearing, detoxifying, and diuretic properties, as well as for treating gastrointestinal disorders such as diarrhea and dysentery. Its reported anti-inflammatory and hemostatic effects are closely linked to inflammatory pathways. While previous studies have demonstrated AAL's efficacy in acute colitis, its therapeutic potential in chronic colitis and the underlying mechanisms remain largely unexplored.</div></div><div><h3>Aim of the study</h3><div>This study aims to investigate the therapeutic efficacy of AAL in dextran sulfate sodium (DSS)-induced chronic colitis and elucidate its anti-inflammatory and barrier-protective mechanisms, with a specific focus on the FABP4/PPARγ/NF-κB signaling pathway.</div></div><div><h3>Materials and methods</h3><div>The chemical composition of AAL was characterized using ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS). Chronic colitis was induced in mice through three cycles of DSS administration, and the therapeutic effects of AAL were evaluated by assessing body weight, Disease Activity Index (DAI), colon length, and pathological alterations. Enzyme-linked immunosorbent assay (ELISA) was used to quantify inflammatory cytokine levels. Immunohistochemistry and Western blotting were performed to assess mucosal barrier proteins, including Mucin 2 (MUC2), zonula occludens-1 (ZO-1), and Occludin, as well as key signaling proteins such as fatty acid-binding protein 4 (FABP4), peroxisome proliferator-activated receptor gamma (PPARγ), and phosphorylated P65 (p-P65). Proteomic analysis combined with Gene Set Enrichment Analysis (GSEA) was conducted to identify differentially expressed proteins and enriched pathways. The role of the FABP4/PPARγ/NF-κB axis was further validated using the PPARγ antagonist GW9662. Additionally, molecular docking and molecular dynamics simulations were employed to identify bioactive components in AAL and their interactions with FABP4 and PPARγ.</div></div><div><h3>Results</h3><div>UPLC-QTOF-MS analysis identified 47 compounds in AAL, including flavonoids, terpenoids, and polyphenols. Bergaptol and corilagin were identified as major constituents with potential anti-inflammatory properties. AAL treatment significantly alleviated chronic colitis symptoms, as evidenced by reduced DAI scores, restoration of body weight, and improved colon length. Pathological and immunohistochemical analyses demonstrated that AAL preserved intestinal mucosal integrity by upregulating MUC2, ZO-1, and Occludin expression. Proteomic and GSEA analyses identified the FABP4/PPARγ/NF-κB pathway as a key target of AAL. Western blotting confirmed that AAL suppressed FABP4 expression, enhanced PPARγ levels, and reduced p-P65 expression, indicating inhibition o
{"title":"Proteomic analysis reveals that Acalypha australis L. mitigates chronic colitis by modulating the FABP4/PPARγ/NF-κB signaling pathway","authors":"Xiaoyu Quan ,&nbsp;Zhiwei Miao ,&nbsp;Runxi Han ,&nbsp;Rui Deng ,&nbsp;Yaqi Cao ,&nbsp;Jingshan Tian ,&nbsp;Yaping Lu ,&nbsp;Guoxiang Wang ,&nbsp;Xingjian Yu ,&nbsp;Yi Wu ,&nbsp;Chen Dai","doi":"10.1016/j.jep.2025.119585","DOIUrl":"10.1016/j.jep.2025.119585","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Ethnopharmacological relevance&lt;/h3&gt;&lt;div&gt;&lt;em&gt;Acalypha australis&lt;/em&gt; L. (AAL), a traditional medicinal herb from the Euphorbiaceae family, has been widely used in Chinese medicine for its heat-clearing, detoxifying, and diuretic properties, as well as for treating gastrointestinal disorders such as diarrhea and dysentery. Its reported anti-inflammatory and hemostatic effects are closely linked to inflammatory pathways. While previous studies have demonstrated AAL's efficacy in acute colitis, its therapeutic potential in chronic colitis and the underlying mechanisms remain largely unexplored.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Aim of the study&lt;/h3&gt;&lt;div&gt;This study aims to investigate the therapeutic efficacy of AAL in dextran sulfate sodium (DSS)-induced chronic colitis and elucidate its anti-inflammatory and barrier-protective mechanisms, with a specific focus on the FABP4/PPARγ/NF-κB signaling pathway.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Materials and methods&lt;/h3&gt;&lt;div&gt;The chemical composition of AAL was characterized using ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS). Chronic colitis was induced in mice through three cycles of DSS administration, and the therapeutic effects of AAL were evaluated by assessing body weight, Disease Activity Index (DAI), colon length, and pathological alterations. Enzyme-linked immunosorbent assay (ELISA) was used to quantify inflammatory cytokine levels. Immunohistochemistry and Western blotting were performed to assess mucosal barrier proteins, including Mucin 2 (MUC2), zonula occludens-1 (ZO-1), and Occludin, as well as key signaling proteins such as fatty acid-binding protein 4 (FABP4), peroxisome proliferator-activated receptor gamma (PPARγ), and phosphorylated P65 (p-P65). Proteomic analysis combined with Gene Set Enrichment Analysis (GSEA) was conducted to identify differentially expressed proteins and enriched pathways. The role of the FABP4/PPARγ/NF-κB axis was further validated using the PPARγ antagonist GW9662. Additionally, molecular docking and molecular dynamics simulations were employed to identify bioactive components in AAL and their interactions with FABP4 and PPARγ.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;UPLC-QTOF-MS analysis identified 47 compounds in AAL, including flavonoids, terpenoids, and polyphenols. Bergaptol and corilagin were identified as major constituents with potential anti-inflammatory properties. AAL treatment significantly alleviated chronic colitis symptoms, as evidenced by reduced DAI scores, restoration of body weight, and improved colon length. Pathological and immunohistochemical analyses demonstrated that AAL preserved intestinal mucosal integrity by upregulating MUC2, ZO-1, and Occludin expression. Proteomic and GSEA analyses identified the FABP4/PPARγ/NF-κB pathway as a key target of AAL. Western blotting confirmed that AAL suppressed FABP4 expression, enhanced PPARγ levels, and reduced p-P65 expression, indicating inhibition o","PeriodicalId":15761,"journal":{"name":"Journal of ethnopharmacology","volume":"345 ","pages":"Article 119585"},"PeriodicalIF":4.8,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Tangshenning formula alleviates tubular injury in diabetic kidney disease via the Sestrin2/AMPK/PGC-1α axis: Restoration of mitochondrial function and inhibition of ferroptosis 丹参宁方通过胰蛋白酶2/AMPK/PGC-1α轴缓解糖尿病肾病的肾小管损伤:恢复线粒体功能和抑制铁氧化酶活性
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-03 DOI: 10.1016/j.jep.2025.119579
Xiao-Meng Shan , Cong Lu , Chun-Wei Chen , Cui-Ting Wang , Tian-Tian Liu , Tian An , Zhi-Yao Zhu , Da-Wei Zou , Yan-Bin Gao

Ethnopharmacological relevance

Tangshenning (TSN) is a traditional Chinese medicinal formula developed on principles of kidney tonification and collateral unblocking. TSN, formulated from Astragalus mongholicus Bunge, Rheum palmatum L., Ligusticum chuanxiong Hort., and Rosa laevigata Michx., has demonstrated significant clinical efficacy in the treatment of diabetic kidney disease (DKD). Our previous studies have suggested that TSN mitigates tubular injury in DKD by inhibiting ferroptosis, however, the precise molecular targets and mechanistic pathways underlying these effects remain to be fully elucidated.

Aim of the study

We investigated whether the Sestrin2/AMPK/PGC-1α axis serves as a key pathway mediating TSN's protective effects against tubular injury in DKD.

Methods

In vivo, a spontaneous DKD mouse model was developed using KK-Ay mice. In vitro, human tubular epithelial cells (TECs) were used to establish high glucose and ferroptosis models, as well as a Sestrin2 knockdown model for further analysis. Molecular docking was utilized to examine the binding interactions between TSN's key active components and Sestrin2. Colocalization of Sestrin2 and GPX4 was assessed using dual fluorescence staining. Protein expression levels related to the Sestrin2/AMPK/PGC-1α pathway, ferroptosis markers (SLC7A11 and GPX4), and the tubular injury marker KIM-1 were quantified via Western blot analysis. In vivo, DHE staining, TUNEL staining, and ferrous ion content measurement were performed to evaluate ferroptosis levels in renal tissue. In vitro, the BODIPY 581/591 C11 probe and ferrous ion assay were used to assess ferroptosis levels in TECs. MitoSOX staining, JC-1 assay, and ATP level measurements were conducted to evaluate mitochondrial function in TECs.

Results

In vivo, our results demonstrated that TSN improved renal function, alleviated tubular injury, and reduced pathological damage in DKD mice. Furthermore, TSN upregulated the protein expression of the Sestrin2/AMPK/PGC-1α axis and decreased ferroptosis-related markers in the DKD mouse model. Similarly, in vitro, TSN enhanced the expression of the Sestrin2/AMPK/PGC-1α pathway, restored mitochondrial function, and inhibited ferroptosis in TECs under high glucose and ferroptosis-inducing conditions. Additionally, downregulation of Sestrin2 impaired the therapeutic effects of TSN.

Conclusion

TSN alleviates tubular injury in DKD by activating the Sestrin2/AMPK/PGC-1α pathway, restoring mitochondrial function, and inhibiting ferroptosis in TECs.
{"title":"Tangshenning formula alleviates tubular injury in diabetic kidney disease via the Sestrin2/AMPK/PGC-1α axis: Restoration of mitochondrial function and inhibition of ferroptosis","authors":"Xiao-Meng Shan ,&nbsp;Cong Lu ,&nbsp;Chun-Wei Chen ,&nbsp;Cui-Ting Wang ,&nbsp;Tian-Tian Liu ,&nbsp;Tian An ,&nbsp;Zhi-Yao Zhu ,&nbsp;Da-Wei Zou ,&nbsp;Yan-Bin Gao","doi":"10.1016/j.jep.2025.119579","DOIUrl":"10.1016/j.jep.2025.119579","url":null,"abstract":"<div><h3>Ethnopharmacological relevance</h3><div>Tangshenning (TSN) is a traditional Chinese medicinal formula developed on principles of kidney tonification and collateral unblocking. TSN, formulated from <em>Astragalus mongholicus</em> Bunge, <em>Rheum palmatum</em> L., <em>Ligusticum chuanxiong</em> Hort., and <em>Rosa laevigata</em> Michx., has demonstrated significant clinical efficacy in the treatment of diabetic kidney disease (DKD). Our previous studies have suggested that TSN mitigates tubular injury in DKD by inhibiting ferroptosis, however, the precise molecular targets and mechanistic pathways underlying these effects remain to be fully elucidated.</div></div><div><h3>Aim of the study</h3><div>We investigated whether the Sestrin2/AMPK/PGC-1α axis serves as a key pathway mediating TSN's protective effects against tubular injury in DKD.</div></div><div><h3>Methods</h3><div>In vivo, a spontaneous DKD mouse model was developed using KK-Ay mice. In vitro, human tubular epithelial cells (TECs) were used to establish high glucose and ferroptosis models, as well as a Sestrin2 knockdown model for further analysis. Molecular docking was utilized to examine the binding interactions between TSN's key active components and Sestrin2. Colocalization of Sestrin2 and GPX4 was assessed using dual fluorescence staining. Protein expression levels related to the Sestrin2/AMPK/PGC-1α pathway, ferroptosis markers (SLC7A11 and GPX4), and the tubular injury marker KIM-1 were quantified via Western blot analysis. In vivo, DHE staining, TUNEL staining, and ferrous ion content measurement were performed to evaluate ferroptosis levels in renal tissue. In vitro, the BODIPY 581/591 C11 probe and ferrous ion assay were used to assess ferroptosis levels in TECs. MitoSOX staining, JC-1 assay, and ATP level measurements were conducted to evaluate mitochondrial function in TECs.</div></div><div><h3>Results</h3><div>In vivo, our results demonstrated that TSN improved renal function, alleviated tubular injury, and reduced pathological damage in DKD mice. Furthermore, TSN upregulated the protein expression of the Sestrin2/AMPK/PGC-1α axis and decreased ferroptosis-related markers in the DKD mouse model. Similarly, in vitro, TSN enhanced the expression of the Sestrin2/AMPK/PGC-1α pathway, restored mitochondrial function, and inhibited ferroptosis in TECs under high glucose and ferroptosis-inducing conditions. Additionally, downregulation of Sestrin2 impaired the therapeutic effects of TSN.</div></div><div><h3>Conclusion</h3><div>TSN alleviates tubular injury in DKD by activating the Sestrin2/AMPK/PGC-1α pathway, restoring mitochondrial function, and inhibiting ferroptosis in TECs.</div></div>","PeriodicalId":15761,"journal":{"name":"Journal of ethnopharmacology","volume":"345 ","pages":"Article 119579"},"PeriodicalIF":4.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Study on the mechanism of Jieduquyuziyin prescription improving the condition of MRL/lpr mice by regulating T cell metabolic reprogramming through the AMPK/mTOR pathway
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-03 DOI: 10.1016/j.jep.2025.119584
Qingmiao Zhu , Yaxue Han , Xiaolong Li , Shuo Huang , Kai Zhao , Zhijun Xie , Yongsheng Fan , Ting Zhao

Ethnopharmacological relevance

Systemic lupus erythematosus (SLE) is an autoimmune disease associated with T cell metabolic reprogramming. The traditional Chinese medicine Jieduquyuziyin prescription (JP) has demonstrated therapeutic efficacy in SLE, yet its mechanisms remain unclear. This study evaluates the therapeutic effects of JP on SLE, focusing on T cell metabolic reprogramming.

Aim of the study

To assess JP's therapeutic effects on SLE and its role in regulating T cell metabolism.

Materials and methods

MRL/lpr mice were treated with JP and assessed for spleen index, serum biochemistry, autoantibodies, urine protein levels, and histopathology. Th17 and Treg proportions were analyzed via flow cytometry. CD4+T cells were evaluated for the Th17/Treg transcription factors and glucose metabolism indicators through ELISA, quantitative real-time PCR, and assay kits. The AMPK/mTOR pathway was investigated using Compound C in vivo and in vitro.

Results

JP alleviated SLE symptoms, promoted Treg differentiation, and inhibited Th17 differentiation, restoring immune balance. JP reduced glycolysis-related metabolites and enzymes in CD4+T cells, including glucose, pyruvate, lactate, Glucose transporters1 (Glut1), Hexokinase2 (HK2), Pyruvate kinase isozyme typeM2 (PKM2), lactic dehydrogenase A (LDHA). JP decreased RORC expression, a key transcription factor for Th17 cells, and increased Foxp3 expression, a key regulator of Treg cells. JP activated AMPK and inhibited mTOR signaling in both mouse and Jurkat cell models.

Conclusions

JP alleviates SLE symptoms by modulating T cell metabolic reprogramming, primarily through inhibiting glycolysis and restoring the Th17/Treg balance via the AMPK/mTOR pathway. These findings underscore the significance of targeting metabolic pathways in the treatment of autoimmune diseases.
{"title":"Study on the mechanism of Jieduquyuziyin prescription improving the condition of MRL/lpr mice by regulating T cell metabolic reprogramming through the AMPK/mTOR pathway","authors":"Qingmiao Zhu ,&nbsp;Yaxue Han ,&nbsp;Xiaolong Li ,&nbsp;Shuo Huang ,&nbsp;Kai Zhao ,&nbsp;Zhijun Xie ,&nbsp;Yongsheng Fan ,&nbsp;Ting Zhao","doi":"10.1016/j.jep.2025.119584","DOIUrl":"10.1016/j.jep.2025.119584","url":null,"abstract":"<div><h3>Ethnopharmacological relevance</h3><div>Systemic lupus erythematosus (SLE) is an autoimmune disease associated with T cell metabolic reprogramming. The traditional Chinese medicine Jieduquyuziyin prescription (JP) has demonstrated therapeutic efficacy in SLE, yet its mechanisms remain unclear. This study evaluates the therapeutic effects of JP on SLE, focusing on T cell metabolic reprogramming.</div></div><div><h3>Aim of the study</h3><div>To assess JP's therapeutic effects on SLE and its role in regulating T cell metabolism.</div></div><div><h3>Materials and methods</h3><div>MRL/lpr mice were treated with JP and assessed for spleen index, serum biochemistry, autoantibodies, urine protein levels, and histopathology. Th17 and Treg proportions were analyzed via flow cytometry. CD4<sup>+</sup>T cells were evaluated for the Th17/Treg transcription factors and glucose metabolism indicators through ELISA, quantitative real-time PCR, and assay kits. The AMPK/mTOR pathway was investigated using Compound C in vivo and in vitro.</div></div><div><h3>Results</h3><div>JP alleviated SLE symptoms, promoted Treg differentiation, and inhibited Th17 differentiation, restoring immune balance. JP reduced glycolysis-related metabolites and enzymes in CD4<sup>+</sup>T cells, including glucose, pyruvate, lactate, Glucose transporters1 (Glut1), Hexokinase2 (HK2), Pyruvate kinase isozyme typeM2 (PKM2), lactic dehydrogenase A (LDHA). JP decreased RORC expression, a key transcription factor for Th17 cells, and increased Foxp3 expression, a key regulator of Treg cells. JP activated AMPK and inhibited mTOR signaling in both mouse and Jurkat cell models.</div></div><div><h3>Conclusions</h3><div>JP alleviates SLE symptoms by modulating T cell metabolic reprogramming, primarily through inhibiting glycolysis and restoring the Th17/Treg balance via the AMPK/mTOR pathway. These findings underscore the significance of targeting metabolic pathways in the treatment of autoimmune diseases.</div></div>","PeriodicalId":15761,"journal":{"name":"Journal of ethnopharmacology","volume":"345 ","pages":"Article 119584"},"PeriodicalIF":4.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143562195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Qingre Huayu Jianpi prescription alleviates the inflammatory transformation of colitis-associated colorectal cancer by inhibiting the IL-17RA/ACT1/NF-κB axis 清热化瘀健脾方通过抑制 IL-17RA/ACT1/NF-κB 轴,缓解结肠炎相关性结直肠癌的炎性转化。
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-03 DOI: 10.1016/j.jep.2025.119554
Yilin Duan , Yao Lu , Zhenglin Liu , Jin Zhang , Zhiyu Yang , Yihan Guo , Yi Yang , Wenjia Lin , Yuxing Shuai , Jiaying Huang , Yingjian Xu , Renxiong Wu , Yongqiang Wu , Yanwu Li , Junyu Ke

Ethnopharmacological relevance

Inflammation-to-cancer transformation is critical for the progression of ulcerative colitis to colitis-associated colorectal cancer (CAC).

Aim of the study

To explore the role and potential mechanisms of Qingre Huayu Jianpi prescription (QHJ) treatment in the development of CAC.

Materials and methods

Combined network pharmacology and transcriptome analyses were used to investigate QHJ-associated targets and pathways in the context of CAC. Using clinical data and a murine CAC model, we examined QHJ effects on pathological morphology, inflammatory factors, and key target pathways.

Results

Network pharmacology analysis identified the interleukin 17 receptor A (IL-17RA)/ACT1/nuclear factor kappa B (NF-κB) axis as critical in the inflammation-to-CAC transformation and for QHJ effects in CAC. Western blot and multiplex immunofluorescence analyses revealed significant upregulation of the IL-17RA/ACT1/NF-κB axis along with matrix metalloproteinase (MMP)7, MMP9, and chemokine ligand 2 (CCL2) in human tumor tissues. QHJ significantly ameliorated CAC-related symptoms in mice in vivo by downregulating the IL-17RA/ACT1/NF-κB axis. This reduced the number of colorectal adenomas, increased colorectal length, and improved the structure of colonic mucosal glands. Additionally, QHJ inhibited the expression of pro-inflammatory factors and decreased the levels of MMP7, MMP9, and CCL2, ultimately suppressing the inflammation-to-cancer transformation.

Conclusion

QHJ exhibited significant therapeutic effects on CAC in mice, likely due to its inhibitory action on the IL-17RA/ACT1/NF-κB axis. This study lays the foundation for research into the pathogenesis of CAC and the clinical application of QHJ.
{"title":"Qingre Huayu Jianpi prescription alleviates the inflammatory transformation of colitis-associated colorectal cancer by inhibiting the IL-17RA/ACT1/NF-κB axis","authors":"Yilin Duan ,&nbsp;Yao Lu ,&nbsp;Zhenglin Liu ,&nbsp;Jin Zhang ,&nbsp;Zhiyu Yang ,&nbsp;Yihan Guo ,&nbsp;Yi Yang ,&nbsp;Wenjia Lin ,&nbsp;Yuxing Shuai ,&nbsp;Jiaying Huang ,&nbsp;Yingjian Xu ,&nbsp;Renxiong Wu ,&nbsp;Yongqiang Wu ,&nbsp;Yanwu Li ,&nbsp;Junyu Ke","doi":"10.1016/j.jep.2025.119554","DOIUrl":"10.1016/j.jep.2025.119554","url":null,"abstract":"<div><h3>Ethnopharmacological relevance</h3><div>Inflammation-to-cancer transformation is critical for the progression of ulcerative colitis to colitis-associated colorectal cancer (CAC).</div></div><div><h3>Aim of the study</h3><div>To explore the role and potential mechanisms of Qingre Huayu Jianpi prescription (QHJ) treatment in the development of CAC.</div></div><div><h3>Materials and methods</h3><div>Combined network pharmacology and transcriptome analyses were used to investigate QHJ-associated targets and pathways in the context of CAC. Using clinical data and a murine CAC model, we examined QHJ effects on pathological morphology, inflammatory factors, and key target pathways.</div></div><div><h3>Results</h3><div>Network pharmacology analysis identified the interleukin 17 receptor A (IL-17RA)/ACT1/nuclear factor kappa B (NF-κB) axis as critical in the inflammation-to-CAC transformation and for QHJ effects in CAC. Western blot and multiplex immunofluorescence analyses revealed significant upregulation of the IL-17RA/ACT1/NF-κB axis along with matrix metalloproteinase (MMP)7, MMP9, and chemokine ligand 2 (CCL2) in human tumor tissues. QHJ significantly ameliorated CAC-related symptoms in mice <em>in vivo</em> by downregulating the IL-17RA/ACT1/NF-κB axis. This reduced the number of colorectal adenomas, increased colorectal length, and improved the structure of colonic mucosal glands. Additionally, QHJ inhibited the expression of pro-inflammatory factors and decreased the levels of MMP7, MMP9, and CCL2, ultimately suppressing the inflammation-to-cancer transformation.</div></div><div><h3>Conclusion</h3><div>QHJ exhibited significant therapeutic effects on CAC in mice, likely due to its inhibitory action on the IL-17RA/ACT1/NF-κB axis. This study lays the foundation for research into the pathogenesis of CAC and the clinical application of QHJ.</div></div>","PeriodicalId":15761,"journal":{"name":"Journal of ethnopharmacology","volume":"345 ","pages":"Article 119554"},"PeriodicalIF":4.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Explore the key targets and mechanism of Danggui Buxue decoction against ulcerative colitis: Network pharmacology and experimental validation
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-03 DOI: 10.1016/j.jep.2025.119580
Wen-Juan Liu , Shan-Bo Ma , Jia-Xin Li , Bei-Sheng Fan , Yan Du , Zhi-Hui Xu , Xiao-Qiang Li , Wei Cao , Yu-Ping Tang

Ethnopharmacological relevance

The traditional Chinese herbal formula, Danggui Buxue decoction (DBD), is known for its ability in tonifying Qi and promoting the production of blood. It is extensively utilized in treating menstrual anemia and chronic non-healing ulcers. Whereas the impact of DBD on ulcerative colitis (UC) has not been explored, and its therapeutic mechanisms are not well comprehended.

Aim of the study

The research sought to investigate the impacts and mechanisms of DBD on UC through a blend of network pharmacology and experimental confirmation.

Materials and methods

A network pharmacology approach was utilized to predict DBD's potential mechanisms of action on UC, which were then validated through experimental studies using a dextran sulfate sodium (DSS)-induced UC mouse model to assess its protective effects on intestinal injury. Western blot analysis was conducted to examine changes in protein expression within the primary pathway affected by DBD.

Results

A total of 27 active chemical components, 265 potential targets, and 5867 UC target genes were identified through screening. Of these, 172 common targets were found between DBD and UC. Additionally, 2359 GO biological process items and 157 KEGG signal pathways were identified through analysis. Molecular docking revealed strong binding ability between the main compounds and target proteins. In the DSS-induced UC mouse model, DBD reduced intestinal inflammation and attenuated colonic pathological damage, which is associated with DBD's inhibition of the PI3K/AKT pathway.

Conclusions

DBD significantly attenuates colonic inflammation and preserves the integrity of the intestinal mucosa. Furthermore, the anti-UC efficacy of DBD is intricately linked to the suppression of the PI3K/AKT pathway.
{"title":"Explore the key targets and mechanism of Danggui Buxue decoction against ulcerative colitis: Network pharmacology and experimental validation","authors":"Wen-Juan Liu ,&nbsp;Shan-Bo Ma ,&nbsp;Jia-Xin Li ,&nbsp;Bei-Sheng Fan ,&nbsp;Yan Du ,&nbsp;Zhi-Hui Xu ,&nbsp;Xiao-Qiang Li ,&nbsp;Wei Cao ,&nbsp;Yu-Ping Tang","doi":"10.1016/j.jep.2025.119580","DOIUrl":"10.1016/j.jep.2025.119580","url":null,"abstract":"<div><h3>Ethnopharmacological relevance</h3><div>The traditional Chinese herbal formula, Danggui Buxue decoction (DBD), is known for its ability in tonifying Qi and promoting the production of blood. It is extensively utilized in treating menstrual anemia and chronic non-healing ulcers. Whereas the impact of DBD on ulcerative colitis (UC) has not been explored, and its therapeutic mechanisms are not well comprehended.</div></div><div><h3>Aim of the study</h3><div>The research sought to investigate the impacts and mechanisms of DBD on UC through a blend of network pharmacology and experimental confirmation.</div></div><div><h3>Materials and methods</h3><div>A network pharmacology approach was utilized to predict DBD's potential mechanisms of action on UC, which were then validated through experimental studies using a dextran sulfate sodium (DSS)-induced UC mouse model to assess its protective effects on intestinal injury. Western blot analysis was conducted to examine changes in protein expression within the primary pathway affected by DBD.</div></div><div><h3>Results</h3><div>A total of 27 active chemical components, 265 potential targets, and 5867 UC target genes were identified through screening. Of these, 172 common targets were found between DBD and UC. Additionally, 2359 GO biological process items and 157 KEGG signal pathways were identified through analysis. Molecular docking revealed strong binding ability between the main compounds and target proteins. In the DSS-induced UC mouse model, DBD reduced intestinal inflammation and attenuated colonic pathological damage, which is associated with DBD's inhibition of the PI3K/AKT pathway.</div></div><div><h3>Conclusions</h3><div>DBD significantly attenuates colonic inflammation and preserves the integrity of the intestinal mucosa. Furthermore, the anti-UC efficacy of DBD is intricately linked to the suppression of the PI3K/AKT pathway.</div></div>","PeriodicalId":15761,"journal":{"name":"Journal of ethnopharmacology","volume":"344 ","pages":"Article 119580"},"PeriodicalIF":4.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143551287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
2,3,5,4′-Tetrahydroxystilbene-2-O-beta-D-glucopyranoside promotes skin flap survival by promoting mitophagy through the PINK1/Parkin pathway
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-03 DOI: 10.1016/j.jep.2025.119587
Weilong Song , Jialong Yang , Kechen Zhang, Panshen Xu, Hebin Pan, Jiapeng Deng, An Wang, Kaitao Wang, Dingsheng Lin

Ethnopharmacological relevance

2,3,5,4′-Tetrahydroxystilbene-2-O-beta-D-glucopyranoside (THSG), the active compound in Polygonum multiflorum (PM), exhibits potential therapeutic effects, including combating oxidative stress, possessing anti-tumor properties, and protecting against ischemia-reperfusion injury. However, the influence and mechanisms by which THSG affects skin flap survival remain unclear.

Aim of study

To investigate the effects and underlying mechanisms of THSG to promote the survival rate of skin flap.

Methods

McFarlane skin flap models were created in 24 Sprague-Dawley rats, which were randomly divided into four groups: control group, low-dose THSG group (30 mg/kg/day), medium-dose THSG group (60 mg/kg/day), and high-dose THSG group (120 mg/kg/day). Seven days after postoperative administration, blood perfusion was assessed using laser Doppler, and the survival rate was calculated. Anti-tumor necrosis factor (TNF)-α was analyzed via immunofluorescence. Interleukin (IL)-6 and IL-1β were explored by enzyme-linked immunosorbent assay (ELISA). SOD activity and MDA contents in skin flap tissue were detected to evaluate oxidative stress level, while Western blotting was employed to assess proteins of the PINK1/Parkin signaling axis, apoptosis-related proteins, and vascular endothelial growth factor (VEGF).

Results

THSG upregulated VEGF expression, improved blood flow, and protected flap tissue by reducing inflammation, mitigating oxidative stress, and inhibiting apoptosis. Increased expression of Parkin and PINK1, along with decreased levels of COX IV, suggested that THSG mediates mitophagy via the PINK1/Parkin signaling pathway.

Conclusions

THSG enhances the survival rate of skin flap by promoting PINK1/Parkin-mediated mitophagy.
{"title":"2,3,5,4′-Tetrahydroxystilbene-2-O-beta-D-glucopyranoside promotes skin flap survival by promoting mitophagy through the PINK1/Parkin pathway","authors":"Weilong Song ,&nbsp;Jialong Yang ,&nbsp;Kechen Zhang,&nbsp;Panshen Xu,&nbsp;Hebin Pan,&nbsp;Jiapeng Deng,&nbsp;An Wang,&nbsp;Kaitao Wang,&nbsp;Dingsheng Lin","doi":"10.1016/j.jep.2025.119587","DOIUrl":"10.1016/j.jep.2025.119587","url":null,"abstract":"<div><h3>Ethnopharmacological relevance</h3><div>2,3,5,4′-Tetrahydroxystilbene-2-O-beta-D-glucopyranoside (THSG), the active compound in <em>Polygonum multiflorum</em> (PM), exhibits potential therapeutic effects, including combating oxidative stress, possessing anti-tumor properties, and protecting against ischemia-reperfusion injury. However, the influence and mechanisms by which THSG affects skin flap survival remain unclear.</div></div><div><h3>Aim of study</h3><div>To investigate the effects and underlying mechanisms of THSG to promote the survival rate of skin flap.</div></div><div><h3>Methods</h3><div>McFarlane skin flap models were created in 24 Sprague-Dawley rats, which were randomly divided into four groups: control group, low-dose THSG group (30 mg/kg/day), medium-dose THSG group (60 mg/kg/day), and high-dose THSG group (120 mg/kg/day). Seven days after postoperative administration, blood perfusion was assessed using laser Doppler, and the survival rate was calculated. Anti-tumor necrosis factor (TNF)-α was analyzed via immunofluorescence. Interleukin (IL)-6 and IL-1β were explored by enzyme-linked immunosorbent assay (ELISA). SOD activity and MDA contents in skin flap tissue were detected to evaluate oxidative stress level, while Western blotting was employed to assess proteins of the PINK1/Parkin signaling axis, apoptosis-related proteins, and vascular endothelial growth factor (VEGF).</div></div><div><h3>Results</h3><div>THSG upregulated VEGF expression, improved blood flow, and protected flap tissue by reducing inflammation, mitigating oxidative stress, and inhibiting apoptosis. Increased expression of Parkin and PINK1, along with decreased levels of COX IV, suggested that THSG mediates mitophagy via the PINK1/Parkin signaling pathway.</div></div><div><h3>Conclusions</h3><div>THSG enhances the survival rate of skin flap by promoting PINK1/Parkin-mediated mitophagy.</div></div>","PeriodicalId":15761,"journal":{"name":"Journal of ethnopharmacology","volume":"345 ","pages":"Article 119587"},"PeriodicalIF":4.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143562184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Corrigendum to “Integration of metabolomics and transcriptomics to reveal the mechanism of Gerberae piloselloidis herba in alleviating bronchial asthma” [J. Ethnopharmacol. 355 (2024) 117852]
IF 4.8 2区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2025-03-03 DOI: 10.1016/j.jep.2025.119523
Chunhua Liu , Changli Fu , Yuan Lu , Jia Sun , Ting Liu , Yonglin Wang , Aimin Wang , Yong Huang , Yongjun Li
{"title":"Corrigendum to “Integration of metabolomics and transcriptomics to reveal the mechanism of Gerberae piloselloidis herba in alleviating bronchial asthma” [J. Ethnopharmacol. 355 (2024) 117852]","authors":"Chunhua Liu ,&nbsp;Changli Fu ,&nbsp;Yuan Lu ,&nbsp;Jia Sun ,&nbsp;Ting Liu ,&nbsp;Yonglin Wang ,&nbsp;Aimin Wang ,&nbsp;Yong Huang ,&nbsp;Yongjun Li","doi":"10.1016/j.jep.2025.119523","DOIUrl":"10.1016/j.jep.2025.119523","url":null,"abstract":"","PeriodicalId":15761,"journal":{"name":"Journal of ethnopharmacology","volume":"344 ","pages":"Article 119523"},"PeriodicalIF":4.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Journal of ethnopharmacology
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