首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Yu Shi An Chang Fang Ameliorates TNBS-Induced Colitis in Mice by Reducing Inflammatory Response and Protecting the Intestinal Mucosal Barrier
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Yu Shi An Chang Fang Ameliorates TNBS-Induced Colitis in Mice by Reducing Inflammatory Response and Protecting the Intestinal Mucosal Barrier

机译:Yu Shi An Chang Fang通过减少炎症反应和保护肠粘膜屏障来改善小鼠的TNBS诱导的结肠炎

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Ulcerative colitis (UC) is an inflammatory bowel disease that is related to the occurrence of colon cancer. This study aimed to investigate the underlying mechanism by which Yu Shi An Chang Fang (YST) treated UC. 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) was used to construct the UC model. The body weight, fecal viscosity, and fecal bleeding of all mice were recorded every day to calculate the DAI value. The pathological changes in colon tissues were observed by hematoxylin-eosin (H&E) staining. The levels of tumor necrosis factor- α (TNF- α ), interleukin-1 beta (IL-1 β ), interleukin-6 (IL-6), and myeloperoxidase (MPO) reflecting inflammation and the levels of malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) reflecting oxidative stress in colon tissues were all measured by their assay kits. The mRNA expression of TNF- α , IL-1 β, and IL-6 in colon tissues was detected by quantitative reverse transcription-PCR (qRT-PCR). The expression of proteins related to pyroptosis and the colonic mucosal barrier was analyzed by Western blot. As a result, TNBS caused decreases in body weight and colon lengths, triggered serious histological damage, promoted inflammation, oxidative stress, and pyroptosis, and destroyed the colonic mucosal barrier. The above changes caused by TNBS in colitis mice could be partially reversed by YST. In conclusion, YST ameliorates TNBS-induced UC in mice by reducing the inflammatory response and protecting the intestinal mucosal barrier.
机译:溃疡性结肠炎(UC)是一种与结肠癌发生有关的炎症性肠病。本研究旨在调查余志张芳(YST)处理的UC的潜在机制。 2,4,4,6-三硝基苯磺酸(TNB)用于构建UC模型。每天记录所有小鼠的体重,粪便粘度和粪便出血以计算傣族价值。通过苏木精 - 曙红(H&E)染色来观察结肠组织的病理变化。肿瘤坏死因子 - α(TNF-α),白细胞介素-1β(IL-1β),白细胞介素-6(IL-6)和髓过氧化物酶(MPO)反映炎症和丙二醛水平(MDA),谷胱甘肽过氧化物酶(GSH-PX)和反映结肠组织中氧化应激的超氧化物歧化酶(SOD)全部通过其测定试剂盒测量。通过定量逆转录-PCR(QRT-PCR)检测结肠组织中TNF-α,IL-1β和IL-6的mRNA表达。用蛋白质印迹分析了与糊酶相关的蛋白质和结肠粘膜屏障的表达。结果,TNB引起体重和结肠长度的降低,引发了严重的组织学损伤,促进炎症,氧化应激和糊酶,并破坏了结肠粘膜屏障。在结肠炎小鼠中由TNB引起的上述变化可以通过YST部分反转。总之,YST通过减少炎症反应和保护肠粘膜屏障来改善小鼠中的TNBS诱导的UC。

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