{"title":"四君子汤治疗溃疡性结肠炎的体外功能实验研究","authors":"Guobao Zhang, Wei Li","doi":"10.4314/tjpr.v22i9.12","DOIUrl":null,"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":0.6000,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"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\":null,\"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\":0.6000,\"publicationDate\":\"2023-10-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Tropical Journal of Pharmaceutical Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4314/tjpr.v22i9.12\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"PHARMACOLOGY & PHARMACY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tropical Journal of Pharmaceutical Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4314/tjpr.v22i9.12","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0
摘要
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。
Therapeutic effect of Sijunzi decoction on ulcerative colitis: A study based on in vitro functional experiments
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.
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