Purpose: To investigate the efficacy of Sijunzi decoction (SJZD) against ulcerative colitis (UC) in vitro, and to unravel the probable mechanism of action.Methods: SEC-6 cells were exposed to lipopolysaccharide (LPS) in order to establish an ulcerative colitis model, and then treated with SJZD. CCK-8 assay was employed to evaluate cell viability, while cell apoptosis was determined by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) were used to assess inflammation factors, viz, TNF-α, IL-1β and IL-6, whereas the expression levels of Bax, Bcl-2 and peroxisome proliferatoractivated receptors (PPARs) were evaluated by Western blot.Results: SJZD doses of 80 and 160 mg/L increased cell viability in LPS-induced SEC-6 cells, while Bcl2 and Bax expressions were regulated, and apoptosis inhibited at these doses (p < 0.05), indicating that SJZD attenuated cell apoptosis. Inflammation was also repressed by SJZD, based on the reduced expressions of TNF-α, IL-1β and IL-6 (p < 0.05). Furthermore, SJZD significantly increased PPARα level, thus enhancing cell viability, inhibiting apoptosis as well as inhibiting inflammation (p < 0.05).Conclusion: SJZD lowers cell damage, and inhibits cell apoptosis and inflammation through the activation of PPARα pathway, thus suggesting that SJZD is a potential therapeutic candidate for the treatment of ulcerative colitis.
目的:观察四君子汤对溃疡性结肠炎(UC)的体外治疗作用，并探讨其可能的作用机制。方法:将SEC-6细胞暴露于脂多糖(LPS)下建立溃疡性结肠炎模型，再用SJZD处理。CCK-8法检测细胞活力，流式细胞术检测细胞凋亡。采用酶联免疫吸附法(ELISA)和实时定量聚合酶链反应(qRT-PCR)检测炎症因子TNF-α、IL-1β和IL-6, Western blot检测Bax、Bcl-2和过氧化物酶体增殖激活受体(PPARs)的表达水平。结果:80、160 mg/L SJZD剂量可提高lps诱导的SEC-6细胞的细胞活力，调节Bcl2和Bax的表达，抑制细胞凋亡(p <0.05)，表明SJZD能减轻细胞凋亡。通过降低TNF-α、IL-1β和IL-6的表达，SJZD也能抑制炎症(p <0.05)。此外，SJZD显著提高PPARα水平，从而提高细胞活力，抑制细胞凋亡，抑制炎症(p <0.05)。结论:SJZD通过激活PPARα通路，降低细胞损伤，抑制细胞凋亡和炎症反应，提示SJZD是治疗溃疡性结肠炎的潜在候选药物。
{"title":"Therapeutic effect of Sijunzi decoction on ulcerative colitis: A study based on in vitro functional experiments","authors":"Guobao Zhang, Wei Li","doi":"10.4314/tjpr.v22i9.12","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.12","url":null,"abstract":"Purpose: To investigate the efficacy of Sijunzi decoction (SJZD) against ulcerative colitis (UC) in vitro, and to unravel the probable mechanism of action.Methods: SEC-6 cells were exposed to lipopolysaccharide (LPS) in order to establish an ulcerative colitis model, and then treated with SJZD. CCK-8 assay was employed to evaluate cell viability, while cell apoptosis was determined by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) were used to assess inflammation factors, viz, TNF-α, IL-1β and IL-6, whereas the expression levels of Bax, Bcl-2 and peroxisome proliferatoractivated receptors (PPARs) were evaluated by Western blot.Results: SJZD doses of 80 and 160 mg/L increased cell viability in LPS-induced SEC-6 cells, while Bcl2 and Bax expressions were regulated, and apoptosis inhibited at these doses (p < 0.05), indicating that SJZD attenuated cell apoptosis. Inflammation was also repressed by SJZD, based on the reduced expressions of TNF-α, IL-1β and IL-6 (p < 0.05). Furthermore, SJZD significantly increased PPARα level, thus enhancing cell viability, inhibiting apoptosis as well as inhibiting inflammation (p < 0.05).Conclusion: SJZD lowers cell damage, and inhibits cell apoptosis and inflammation through the activation of PPARα pathway, thus suggesting that SJZD is a potential therapeutic candidate for the treatment of ulcerative colitis.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"61 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To evaluate the mechanism and effect of Procyanidin A1 (PCA1) in gestational diabetes mellitus (GDM).Methods: Human trophoblast cell line HTR-8/Svneo was treated with 25 mM glucose for 24 h, and the effect of PCA1 on HTR-8/SVneo cell viability and proliferation was determined by CCK-8 assay and EdU proliferation kit. The expression of BAX, Bcl-2, cleaved Caspase-3 and cleaved caspase-9 was determined by western blotting. Cell apoptosis was assessed by Annexin V-FITC/ PI staining. Cellular generation of reactive oxygen species (ROS) was determined by ROS assay kit while superoxide dismutase (SOD), malondialdehyde (MDA), and catalase (CAT) were determined by the corresponding assay kits. The effect of PCA1 on Nrf2/HO-1 pathway was evaluated by determining the expression of Keap1, Nfr2, and HO-1.Results: Procyanidin A1 (PCA1) increased the viability of high glucose (HG) -induced HTR-8/SVneo cells and promoted cell proliferation. Furthermore, PCA1 significantly inhibited HG-induced BAX, cleaved caspase-3, and cleaved caspase-9 expression, resulting in further reduction in HG-induced cell apoptosis. High glucose (HG) induced a significant increase in intracellular ROS levels, and this HGinduced oxidative stress was inhibited by PCA1. Furthermore, PCA1 activated Nrf2/HO-1 pathway and this was responsible for its proliferative, anti-apoptosis and anti-oxidative effects.Conclusion: Procyanidin A1 promotes proliferation, and inhibits apoptosis and oxidative stress induced by high glucose in trophoblast cells by activating Nrf2/HO-1 signaling pathway. Therefore, it is a potential drug for the treatment of GDM.
{"title":"Procyanidin A1 acts as an antioxidant stressor in gestational diabetes","authors":"Mengni Zhu, Liping Liu","doi":"10.4314/tjpr.v22i9.13","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.13","url":null,"abstract":"Purpose: To evaluate the mechanism and effect of Procyanidin A1 (PCA1) in gestational diabetes mellitus (GDM).Methods: Human trophoblast cell line HTR-8/Svneo was treated with 25 mM glucose for 24 h, and the effect of PCA1 on HTR-8/SVneo cell viability and proliferation was determined by CCK-8 assay and EdU proliferation kit. The expression of BAX, Bcl-2, cleaved Caspase-3 and cleaved caspase-9 was determined by western blotting. Cell apoptosis was assessed by Annexin V-FITC/ PI staining. Cellular generation of reactive oxygen species (ROS) was determined by ROS assay kit while superoxide dismutase (SOD), malondialdehyde (MDA), and catalase (CAT) were determined by the corresponding assay kits. The effect of PCA1 on Nrf2/HO-1 pathway was evaluated by determining the expression of Keap1, Nfr2, and HO-1.Results: Procyanidin A1 (PCA1) increased the viability of high glucose (HG) -induced HTR-8/SVneo cells and promoted cell proliferation. Furthermore, PCA1 significantly inhibited HG-induced BAX, cleaved caspase-3, and cleaved caspase-9 expression, resulting in further reduction in HG-induced cell apoptosis. High glucose (HG) induced a significant increase in intracellular ROS levels, and this HGinduced oxidative stress was inhibited by PCA1. Furthermore, PCA1 activated Nrf2/HO-1 pathway and this was responsible for its proliferative, anti-apoptosis and anti-oxidative effects.Conclusion: Procyanidin A1 promotes proliferation, and inhibits apoptosis and oxidative stress induced by high glucose in trophoblast cells by activating Nrf2/HO-1 signaling pathway. Therefore, it is a potential drug for the treatment of GDM.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"24 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135250937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To determine the effect of activating blood circulation and removing blood stasis on the recurrence of alcoholic acute pancreatitis (AAP), and its possible mechanism.Methods: Sixty healthy rats were selected and assigned to control, model and treatment groups (n =20/group). Treatment group was given Taohong Siwu decoction, while control and model groups were given abdominal injection of 0.9 % normal saline. Serum levels of amylase, pancreatic histopathological score, col Ⅰ content, mRNA expression levels of TGF-β 1, TβRII, and Smad3, as well as sPLA2 activity, were determined.Results: Serum amylase, pancreatic histopathological score and col Ⅰ content were significantly reduced in treatment group, relative to model group, while relative mRNA expressions of TGF- β 1, TβRII and Smad3 at each time point were significantly lower than those in the model group (p < 0.05). Serum PLA2 activity and sPLA2 - π a mRNA expression were significantly lower than those in the model group (p < 0.05).Conclusion: Activation of blood circulation and removal of blood stasis significantly prevents the relapse of AAP in rats through regulation of PLA2 activity and TGF-β1/TβRII/Smad3 signaling pathway. Cohort studies in humans would be required to confirm the application of Taohong Siwu decoction to prevent recurrence of AAP.
{"title":"Effect of activating blood circulation and removing blood stasis on recurrence of alcoholic acute pancreatitis, and the possible underlying mechanism","authors":"Haicheng Dong, Weixing Ying, Shifeng Zhu","doi":"10.4314/tjpr.v22i9.11","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.11","url":null,"abstract":"Purpose: To determine the effect of activating blood circulation and removing blood stasis on the recurrence of alcoholic acute pancreatitis (AAP), and its possible mechanism.Methods: Sixty healthy rats were selected and assigned to control, model and treatment groups (n =20/group). Treatment group was given Taohong Siwu decoction, while control and model groups were given abdominal injection of 0.9 % normal saline. Serum levels of amylase, pancreatic histopathological score, col Ⅰ content, mRNA expression levels of TGF-β 1, TβRII, and Smad3, as well as sPLA2 activity, were determined.Results: Serum amylase, pancreatic histopathological score and col Ⅰ content were significantly reduced in treatment group, relative to model group, while relative mRNA expressions of TGF- β 1, TβRII and Smad3 at each time point were significantly lower than those in the model group (p < 0.05). Serum PLA2 activity and sPLA2 - π a mRNA expression were significantly lower than those in the model group (p < 0.05).Conclusion: Activation of blood circulation and removal of blood stasis significantly prevents the relapse of AAP in rats through regulation of PLA2 activity and TGF-β1/TβRII/Smad3 signaling pathway. Cohort studies in humans would be required to confirm the application of Taohong Siwu decoction to prevent recurrence of AAP.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"46 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To evaluate the impact of entecavir (ENT) on patients with liver fibrosis resulting from chronic hepatitis B (CHB) and its association with the interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3)/suppressor of cytokine signaling 3 (SOCS3) pathway.Methods: Thirty-one patients with liver fibrosis received ENT at a dose of 0.5 mg/day for 48 weeks. Relevant protein levels in patient’s serum before and after treatment were assayed using enzyme-linked immunosorbent assay (ELISA). Furthermore, human hepatic stellate cells (HSCs) were cultured in vitro and divided into three groups: control, transforming growth factor beta 1 (TGF-β1) induction (TGF-β1 group), and ENT treatment (TGF-β1 + ENT group). Protein levels in the supernatant were assayed using ELISA, while the expression levels of related genes were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Expression of α-SMA was visualized using immunofluorescence assay and the relevant protein levels were determined by Western blotting.Results: Treatment with ENT significantly decreased (p < 0.01) IL-6 and STAT3 expression, increased SOCS3 expression and significantly reduced (p < 0.01) the concentrations of hyaluronic acid (HA), type IV collagen (IVC), laminin (LN) and pro-collagen type III (PCIII) in patients with liver fibrosis. TGF-β1 significantly (p < 0.01) elevated IL-6, STAT3 and Col-I expressions and a tissue inhibitor of metalloproteinases-1 (TIMP-1) suppressed the expression of SOCS3 in human HSCs and induced fibrosis. Entecavir mitigated TGF-β1-induced fibrogenesis in HSCs (p < 0.01).Conclusion: Entecavir has a positive effect on liver fibrosis resulting from CHB by regulating IL- 6/STAT3/SOCS3 pathway. Future research will focus on conducting larger clinical trials to further validate these findings and explore the long-term effects of ENT on liver fibrosis progression and patient outcomes.
{"title":"Effect of entecavir on IL-6/STAT3/SOCS3 pathway in patients with chronic hepatitis B-induced liver fibrosis","authors":"Shuqiao Wang, Ziqi Sui, Kaili Peng, Hefei Cheng","doi":"10.4314/tjpr.v22i9.22","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.22","url":null,"abstract":"Purpose: To evaluate the impact of entecavir (ENT) on patients with liver fibrosis resulting from chronic hepatitis B (CHB) and its association with the interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3)/suppressor of cytokine signaling 3 (SOCS3) pathway.Methods: Thirty-one patients with liver fibrosis received ENT at a dose of 0.5 mg/day for 48 weeks. Relevant protein levels in patient’s serum before and after treatment were assayed using enzyme-linked immunosorbent assay (ELISA). Furthermore, human hepatic stellate cells (HSCs) were cultured in vitro and divided into three groups: control, transforming growth factor beta 1 (TGF-β1) induction (TGF-β1 group), and ENT treatment (TGF-β1 + ENT group). Protein levels in the supernatant were assayed using ELISA, while the expression levels of related genes were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Expression of α-SMA was visualized using immunofluorescence assay and the relevant protein levels were determined by Western blotting.Results: Treatment with ENT significantly decreased (p < 0.01) IL-6 and STAT3 expression, increased SOCS3 expression and significantly reduced (p < 0.01) the concentrations of hyaluronic acid (HA), type IV collagen (IVC), laminin (LN) and pro-collagen type III (PCIII) in patients with liver fibrosis. TGF-β1 significantly (p < 0.01) elevated IL-6, STAT3 and Col-I expressions and a tissue inhibitor of metalloproteinases-1 (TIMP-1) suppressed the expression of SOCS3 in human HSCs and induced fibrosis. Entecavir mitigated TGF-β1-induced fibrogenesis in HSCs (p < 0.01).Conclusion: Entecavir has a positive effect on liver fibrosis resulting from CHB by regulating IL- 6/STAT3/SOCS3 pathway. Future research will focus on conducting larger clinical trials to further validate these findings and explore the long-term effects of ENT on liver fibrosis progression and patient outcomes.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"67 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To investigate the underlying mechanisms of action of YuShu Soup in exertional heatstroke (EHS) treatment.Methods: This study utilized network pharmacology analysis, applied STRING database to collect compound targets, and visualized protein-protein interaction (PPI) network. Furthermore, EHS model was established on rats, and physiological indices and serum biochemical indicators were evaluated. Thereafter, morphological and histological assessments were carried out on renal tissues.Results: The PPI network indicated that JUN, AKT1, MAPK3, MAPK1, STAT3, RXRA, CTNNB1, and RELA may be the vital proteins which YuShu Soup acts on. In terms of mechanism, YuShu Soup regulates the protein expression of HSP90 and Akt/Bcl-xL pathway significantly (p < 0.01).Conclusion: YuShu Soup alleviates symptoms of EHS and apoptosis of renal cells in rats by regulating HSP90 and Akt/Bcl-xL pathway, thereby alleviating kidney damage. These findings shed light on the prevention and treatment of EHS with this traditional Chinese prescription.
{"title":"Network pharmacology study on mechanism involved in the use of YuShu Soup for the treatment of exertional heatstroke","authors":"Jing Dong, Zheng Yang, Chen Fan","doi":"10.4314/tjpr.v22i9.6","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.6","url":null,"abstract":"Purpose: To investigate the underlying mechanisms of action of YuShu Soup in exertional heatstroke (EHS) treatment.Methods: This study utilized network pharmacology analysis, applied STRING database to collect compound targets, and visualized protein-protein interaction (PPI) network. Furthermore, EHS model was established on rats, and physiological indices and serum biochemical indicators were evaluated. Thereafter, morphological and histological assessments were carried out on renal tissues.Results: The PPI network indicated that JUN, AKT1, MAPK3, MAPK1, STAT3, RXRA, CTNNB1, and RELA may be the vital proteins which YuShu Soup acts on. In terms of mechanism, YuShu Soup regulates the protein expression of HSP90 and Akt/Bcl-xL pathway significantly (p < 0.01).Conclusion: YuShu Soup alleviates symptoms of EHS and apoptosis of renal cells in rats by regulating HSP90 and Akt/Bcl-xL pathway, thereby alleviating kidney damage. These findings shed light on the prevention and treatment of EHS with this traditional Chinese prescription.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"9 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chaosheng Zeng, Huaijie Xing, Min Chen, Lin Chen, Pengxiang Li, Xiaowen Wu, Shaozhu Huang
Purpose: To investigate the use and applications of Internet cloud technology to construct a network management model for statin therapy in Alzheimer’s disease in Hainan Province.Method: Randomized controlled trials (RCTs) investigating the prevention and treatment of Alzheimer's disease (AD) with statins were employed in this study. Computerized searches were conducted using PubMed, EM-BASE, Cochrane Library, Chinese National Knowledge Infrastructure (CNKI), WANFANG Data, and Curriculum-Based Measurement (CBM) retrieval systems, with a retrieval timeframe of April 2012. After literature screening, data extraction, and quality evaluation, Meta-analysis was performed using Review Manager 5.1.0 software.Results: A total of 827 publications were obtained, and 3 RCTs were included after the full texts were studied. While there was no significant advantage of statin use at 3 and 6 months after intervention, the study group exhibited higher Mini-Mental State Examination (MMSE) scores than the control group one year later (p < 0.05). Also, statin use did not have a significant effect on Activities of Daily Living (ADL) scores one year after intervention (p < 0.05). The occurrence of adverse reactions in the two groups was not statistically significant (p > 0.05).Conclusion: The use of Internet cloud technology for building an Alzheimer’s disease network management system simplifies the process of Alzheimer’s disease diagnosis and treatment, and reduces the cost of Alzheimer’s disease services.
{"title":"Utilizing cloud-based technology to construct a precise network management model for statin therapy in Alzheimer's disease - A meta-analysis","authors":"Chaosheng Zeng, Huaijie Xing, Min Chen, Lin Chen, Pengxiang Li, Xiaowen Wu, Shaozhu Huang","doi":"10.4314/tjpr.v22i9.30","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.30","url":null,"abstract":"Purpose: To investigate the use and applications of Internet cloud technology to construct a network management model for statin therapy in Alzheimer’s disease in Hainan Province.Method: Randomized controlled trials (RCTs) investigating the prevention and treatment of Alzheimer's disease (AD) with statins were employed in this study. Computerized searches were conducted using PubMed, EM-BASE, Cochrane Library, Chinese National Knowledge Infrastructure (CNKI), WANFANG Data, and Curriculum-Based Measurement (CBM) retrieval systems, with a retrieval timeframe of April 2012. After literature screening, data extraction, and quality evaluation, Meta-analysis was performed using Review Manager 5.1.0 software.Results: A total of 827 publications were obtained, and 3 RCTs were included after the full texts were studied. While there was no significant advantage of statin use at 3 and 6 months after intervention, the study group exhibited higher Mini-Mental State Examination (MMSE) scores than the control group one year later (p < 0.05). Also, statin use did not have a significant effect on Activities of Daily Living (ADL) scores one year after intervention (p < 0.05). The occurrence of adverse reactions in the two groups was not statistically significant (p > 0.05).Conclusion: The use of Internet cloud technology for building an Alzheimer’s disease network management system simplifies the process of Alzheimer’s disease diagnosis and treatment, and reduces the cost of Alzheimer’s disease services.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"52 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To investigate the effect of Jaceosidin in ulcerative colitis (UC).Methods: An ulcerative colitis cell model was established by stimulating normal human colon mucosal epithelial cell lines (NCM460 cells) with lipopolysaccharide (LPS). The cells were treated with 5, 10, 20 or 40 μM Jaceosidin. Cell viability was performed using cell counting kit 8 (CCK8) assay. Oxidative stress was measured with superoxide dismutase (SOD), lipid peroxidation MDA, reduced glutathione (GSH), oxidized glutathione (GSSG), and human myeloperoxidase enzyme-linked immunoassay (ELISA) kits. The mRNA levels were determined by quantitative polymerase chain reaction (qPCR) assay, while protein levels of SIRT1, NRF2, NLRP3, caspase-1, TNF-α, IL-1β, and IL-6 were determined by western blotting.Results: Jaceosidin significantly inhibited oxidative stress and accumulation of inflammatory cytokines in LPS-induced NCM460 cells, as well as NLRP3-mediated cell pyroptosis (p < 0.05). Jaceosidin also inhibited activation of NLRP3 inflammasome by activating SIRT1/NRF2 pathway, thereby preventing NCM460 cell pyroptosis.Conclusion: Jaceosidin inhibits NLRP3-mediated pyroptosis, thus suggesting that jaceosidin is a potential lead for UC secondary to NLRP3 inflammasome.
{"title":"Jaceosidin inhibits NLRP3-mediated pyroptosis by activating SIRT1/NRF2 and ameliorating intestinal epithelial cell injury","authors":"Yifei Lv, Ting Qiu, Lu Niu","doi":"10.4314/tjpr.v22i9.2","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.2","url":null,"abstract":"Purpose: To investigate the effect of Jaceosidin in ulcerative colitis (UC).Methods: An ulcerative colitis cell model was established by stimulating normal human colon mucosal epithelial cell lines (NCM460 cells) with lipopolysaccharide (LPS). The cells were treated with 5, 10, 20 or 40 μM Jaceosidin. Cell viability was performed using cell counting kit 8 (CCK8) assay. Oxidative stress was measured with superoxide dismutase (SOD), lipid peroxidation MDA, reduced glutathione (GSH), oxidized glutathione (GSSG), and human myeloperoxidase enzyme-linked immunoassay (ELISA) kits. The mRNA levels were determined by quantitative polymerase chain reaction (qPCR) assay, while protein levels of SIRT1, NRF2, NLRP3, caspase-1, TNF-α, IL-1β, and IL-6 were determined by western blotting.Results: Jaceosidin significantly inhibited oxidative stress and accumulation of inflammatory cytokines in LPS-induced NCM460 cells, as well as NLRP3-mediated cell pyroptosis (p < 0.05). Jaceosidin also inhibited activation of NLRP3 inflammasome by activating SIRT1/NRF2 pathway, thereby preventing NCM460 cell pyroptosis.Conclusion: Jaceosidin inhibits NLRP3-mediated pyroptosis, thus suggesting that jaceosidin is a potential lead for UC secondary to NLRP3 inflammasome.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To examine the effectiveness and safety of ultrasound-guided platelet-rich plasma (PRP) injection versus sodium hyaluronate injection in patients with knee osteoarthritis (KOA).Methods: The clinical data of 92 patients treated at the West China Hospital Sichuan University-Ziyang Hospital between May 2020 and December 2021 were retrospectively analyzed. Patients were allocated to PRP group (ultrasound-guided PRP injection) and a hyaluronic acid (HA) group (sodium hyaluronate injection) with each group containing 46 patients. Before and after treatment, the two groups were compared in terms of visual analog scale (VAS) score, Lysholm score, levels of serum inflammatory factors, insulin-like growth factor (IGF)-1, fibroblast growth factor (FGF)-2 and WOMAC score.Results: After treatment, PRP group exhibited significantly lower pain scores and higher function scores than HA group. Furthermore, PRP group exhibited lower levels of inflammation markers, higher levels of growth factors as well as better treatment efficiency and incidence of adverse reactions when compared with HA group (p < 0.05).Conclusion: Ultrasound-guided PRP therapy ameliorates pains and joint functions in KOA patients. The therapeutic effect may be associated with the regulation of cartilage performance and alleviation of inflammatory state. Therefore, PRP injection therapy combined with ultrasound guidance might also have clinical potential for other applications.
{"title":"Effectiveness and safety of an ultrasound-guided injection of platelet-rich plasma versus sodium hyaluronate in patients with knee osteoarthritis","authors":"Wenxing Ding, Qinghua Zhao, Dexiang Zhang, Xiao Zhong","doi":"10.4314/tjpr.v22i9.17","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.17","url":null,"abstract":"Purpose: To examine the effectiveness and safety of ultrasound-guided platelet-rich plasma (PRP) injection versus sodium hyaluronate injection in patients with knee osteoarthritis (KOA).Methods: The clinical data of 92 patients treated at the West China Hospital Sichuan University-Ziyang Hospital between May 2020 and December 2021 were retrospectively analyzed. Patients were allocated to PRP group (ultrasound-guided PRP injection) and a hyaluronic acid (HA) group (sodium hyaluronate injection) with each group containing 46 patients. Before and after treatment, the two groups were compared in terms of visual analog scale (VAS) score, Lysholm score, levels of serum inflammatory factors, insulin-like growth factor (IGF)-1, fibroblast growth factor (FGF)-2 and WOMAC score.Results: After treatment, PRP group exhibited significantly lower pain scores and higher function scores than HA group. Furthermore, PRP group exhibited lower levels of inflammation markers, higher levels of growth factors as well as better treatment efficiency and incidence of adverse reactions when compared with HA group (p < 0.05).Conclusion: Ultrasound-guided PRP therapy ameliorates pains and joint functions in KOA patients. The therapeutic effect may be associated with the regulation of cartilage performance and alleviation of inflammatory state. Therefore, PRP injection therapy combined with ultrasound guidance might also have clinical potential for other applications.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"40 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135250942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To determine the potential cardioprotective effect of vitamin D (VD) against methotrexate (MTX) induced cardiotoxicity.Methods: A total of thirty-five (35) rats were randomly assigned to five equal groups. Control groupreceived no treatment; MTX group received intraperitoneal (IP) injection of MTX in a single dose of 20 mg/kg on day 8; VD group received 200 IU/kg VD daily dissolved in sunflower oil orally; sunflower oil (SO) group received 1 mL/kg/day SO orally; MTX + VD group received a single dose of MTX (20 mg/kg, IP) on day 8 and VD (200 IU/kg, orally) for 21 days. Myocardial tissue samples were harvested and used for clinical chemistry, histopathological, and ultrastructural evaluation.Results: Histopathological damage in MTX group was more severe than in control group under both light and electron microscopy. Expression of transient receptor potential melastatin 2 (TRPM2) and caspase-3 markers was significantly higher in MTX group (p < 0.05). Glutathione peroxidase (GSH-Px) enzyme activity in cardiac tissue was lower in MTX group, whereas malondialdehyde (MDA) levels increased significantly (p < 0.05). In MTX + VD group, VD treatment alleviated histopathological damage and significantly lowered TRPM2 and caspase-3 expressions (p < 0.05). Vitamin D also reduced tissue MDA levels, and increased GSH-Px activity albeit non-significantly (p > 0.05),Conclusion: These findings suggest that VD exerts an ameliorative effect on MTX-induced cardiotoxicity in rats. Therefore, TRPM2 channel affords a novel therapeutic approach for treatment of diseases related to chemotherapy-induced oxidative stress.
{"title":"Vitamin D: An effective therapy against methotrexateinduced cardiotoxicity","authors":"Tuba Ozcan Metin, Alper Yalcin","doi":"10.4314/tjpr.v22i9.10","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.10","url":null,"abstract":"Purpose: To determine the potential cardioprotective effect of vitamin D (VD) against methotrexate (MTX) induced cardiotoxicity.Methods: A total of thirty-five (35) rats were randomly assigned to five equal groups. Control groupreceived no treatment; MTX group received intraperitoneal (IP) injection of MTX in a single dose of 20 mg/kg on day 8; VD group received 200 IU/kg VD daily dissolved in sunflower oil orally; sunflower oil (SO) group received 1 mL/kg/day SO orally; MTX + VD group received a single dose of MTX (20 mg/kg, IP) on day 8 and VD (200 IU/kg, orally) for 21 days. Myocardial tissue samples were harvested and used for clinical chemistry, histopathological, and ultrastructural evaluation.Results: Histopathological damage in MTX group was more severe than in control group under both light and electron microscopy. Expression of transient receptor potential melastatin 2 (TRPM2) and caspase-3 markers was significantly higher in MTX group (p < 0.05). Glutathione peroxidase (GSH-Px) enzyme activity in cardiac tissue was lower in MTX group, whereas malondialdehyde (MDA) levels increased significantly (p < 0.05). In MTX + VD group, VD treatment alleviated histopathological damage and significantly lowered TRPM2 and caspase-3 expressions (p < 0.05). Vitamin D also reduced tissue MDA levels, and increased GSH-Px activity albeit non-significantly (p > 0.05),Conclusion: These findings suggest that VD exerts an ameliorative effect on MTX-induced cardiotoxicity in rats. Therefore, TRPM2 channel affords a novel therapeutic approach for treatment of diseases related to chemotherapy-induced oxidative stress.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"62 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135250943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To assess the therapeutic effects of linarin on chemotherapy-induced peripheral neuropathy (CINP) in rats.Methods: A CINP rat model was established using oxaliplatin. The rats were divided into control, CINP, and two linarin treatment groups (20 mg/kg/day and 40 mg/kg/day). Observations were made at various time points, assessing weight gain, mechanical withdrawal thresholds, cold allodynia response, and thermal pain sensitivity. Additionally, the expression levels of various inflammatory factors (IL-1β, IL-6, IL-10, and IL-17), proteins related to glial and neuronal activation (IBA-1, GFAP, c-fos), and proteins linked to NF-κB/NLRP3 signaling (ASC, caspase-1, p65, and p-p65) were evaluated in rat spinal cord tissue.Results: Linarin treatment resulted in improved weight gain, mechanical threshold, decreased withdrawal response, and enhanced paw withdrawal latency (p < 0.001) compared to the CINP group. These improvements or mitigations were more pronounced in the 40 mg/kg/day linarin group. Linarin inhibited the expression of inflammatory factors IL-1β, IL-6, and IL-17 (p < 0.001) but enhanced IL-10 expression (p < 0.001). The activation of microglia, astrocytes, and neurons, as indicated by IBA-1, GFAP, and c-fos (p < 0.001) proteins, was significantly reduced with linarin, especially at the higher dose. Linarin also suppressed the expression of ASC, caspase-1, p65, and p-p65 (p < 0.001) proteins, associated with the NF-κB/NLRP3 signaling pathway.Conclusion: Our study indicates that linarin may serve as a potential therapeutic agent for managing CINP. The beneficial effects of linarin are likely mediated through its immunomodulatory effects and the inhibition of the NF-κB/NLRP3 signaling pathway. Further research is needed to confirm these findings in clinical settings.
{"title":"Linarin attenuates oxaliplatin-induced neuropathic pain by inhibiting NF-κB/NLRP3 signaling pathway","authors":"Siyu Zeng, Chenming Ling, Hao Chen, Yu Wang","doi":"10.4314/tjpr.v22i9.5","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.5","url":null,"abstract":"Purpose: To assess the therapeutic effects of linarin on chemotherapy-induced peripheral neuropathy (CINP) in rats.Methods: A CINP rat model was established using oxaliplatin. The rats were divided into control, CINP, and two linarin treatment groups (20 mg/kg/day and 40 mg/kg/day). Observations were made at various time points, assessing weight gain, mechanical withdrawal thresholds, cold allodynia response, and thermal pain sensitivity. Additionally, the expression levels of various inflammatory factors (IL-1β, IL-6, IL-10, and IL-17), proteins related to glial and neuronal activation (IBA-1, GFAP, c-fos), and proteins linked to NF-κB/NLRP3 signaling (ASC, caspase-1, p65, and p-p65) were evaluated in rat spinal cord tissue.Results: Linarin treatment resulted in improved weight gain, mechanical threshold, decreased withdrawal response, and enhanced paw withdrawal latency (p < 0.001) compared to the CINP group. These improvements or mitigations were more pronounced in the 40 mg/kg/day linarin group. Linarin inhibited the expression of inflammatory factors IL-1β, IL-6, and IL-17 (p < 0.001) but enhanced IL-10 expression (p < 0.001). The activation of microglia, astrocytes, and neurons, as indicated by IBA-1, GFAP, and c-fos (p < 0.001) proteins, was significantly reduced with linarin, especially at the higher dose. Linarin also suppressed the expression of ASC, caspase-1, p65, and p-p65 (p < 0.001) proteins, associated with the NF-κB/NLRP3 signaling pathway.Conclusion: Our study indicates that linarin may serve as a potential therapeutic agent for managing CINP. The beneficial effects of linarin are likely mediated through its immunomodulatory effects and the inhibition of the NF-κB/NLRP3 signaling pathway. Further research is needed to confirm these findings in clinical settings.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"36 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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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