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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Si Shen Wan Inhibits mRNA Expression of Apoptosis-Related Molecules in p38 MAPK Signal Pathway in Mice with Colitis
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Si Shen Wan Inhibits mRNA Expression of Apoptosis-Related Molecules in p38 MAPK Signal Pathway in Mice with Colitis

机译:四神丸抑制结肠炎小鼠p38 MAPK信号通路中凋亡相关分子的mRNA表达

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Si Shen Wan (SSW) is used to effectively treat ulcerative colitis (UC) as a formula of traditional Chinese medicine. To explore the mechanism of SSW-inhibited apoptosis of colonic epithelial cell, the study observed mRNA expression of apoptosis-related molecules in p38 MAPK signal pathway in colonic mucosa in colitis mice treated with SSW. Experimental colitis was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice; meanwhile, the mice were administrated daily either SSW (5 g/kg) or p38 MAPK inhibitor (2 mg/kg) or vehicle (physiological saline) for 10 days. While microscopical evaluation was observed, apoptosis rate of colonic epithelial cell and mRNA expression of apoptosis-related molecules were tested. Compared with colitis mice without treatment, SSW alleviated colonic mucosal injuries and decreased apoptosis rate of colonic epithelial cell, while the mRNA expressions of p38 MAPK, p53, caspase-3, c-jun, c-fos, Bax, and TNF-αwere decreased in the colonic mucosa in colitis mice treated with SSW, and Bcl-2 mRNA and the ratio of Bcl-2/Bax were increased. The present study demonstrated that SSW inhibited mRNA expression of apoptosis-related molecules in p38 MAPK signal pathway to downregulate colonic epithelial cells apoptosis in colonic mucosa in mice with colitis.
机译:四神丸(SSW)被用作治疗溃疡性结肠炎(UC)的传统中药配方。为了探讨SSW抑制结肠上皮细胞凋亡的机制,该研究观察了用SSW处理的结肠炎小鼠结肠黏膜中p38 MAPK信号途径中凋亡相关分子的mRNA表达。 2,4,6-三硝基苯磺酸(TNBS)在小鼠中诱发实验性结肠炎;同时,每天给小鼠施用SSW(5μg/ kg)或p38 MAPK抑制剂(2μmg/ kg)或溶媒(生理盐水)10天。观察显微镜观察,检测结肠上皮细胞的凋亡率和凋亡相关分子的mRNA表达。与未治疗的结肠炎小鼠相比,SSW减轻了结肠粘膜损伤并降低了结肠上皮细胞的凋亡率,而p38 MAPK,p53,caspase-3,c-jun,c-fos,Bax和TNF-α的mRNA表达降低了。 SSW处理后的结肠炎小鼠结肠黏膜中的Bcl-2 mRNA和Bcl-2 / Bax的比例增加。本研究表明,SSW抑制结肠炎小鼠结肠黏膜中p38 MAPK信号通路中凋亡相关分子的mRNA表达,从而下调结肠黏膜上皮细胞的凋亡。

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