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[黄芩汤对溃疡性结肠炎大鼠调节性NF-κB p65信号通路的影响]

[Effect of huangqin tang on the regulatory NF-κB p65 signal pathway in rats with ulcerative colitis].

作者信息

Wang Yi-wei, Zhang Hui-hui, Wang Yan-li, Guo Shian-shan, Li Tao, Chen Li, Zhuang Shuai-xing, Zhou Zhong-ming, Yang Wei-peng

出版信息

Yao Xue Xue Bao. 2015 Jan;50(1):21-7.

PMID:25924470
Abstract

To investigate the effect of huangqin tang on expression of cytokines and NF-κB p65 in rats with ulcerative colitis (UC), and to probe into its underlying mechanisms of action. The mode of UC rats with cell immunoreactivity was made using compound method (trinitrobenzene sulfonic acid and ethanol). Rats were randomly divided into control group, model group, SASP group and high dose, middle dose and low dose of huangqin tang group. The food intake, body weight and microscopic damage of rats in each group were evaluated after being treated for five days. The blood and colon tissue were also collected. Production of NO was detected by Griess assay, the expression levels of IL-6, TNF-α, PGE2 were detected by ELISA. ICH method was undertaken to determine the expression of NF-κB p65 protein in colon tissue. The food intake and body weight of model group rats were lower than that of control group. The expression levels of NO, IL-6, TNF-α, PGE2 in serum and NF-κB p65 protein of colon tissue in model group were higher than that of control group. The above indexes were ameliorated in high and middle dose of huangqin tang groups. But there was no significant difference with SASP group. NF-κB p65 may be involved in the pathogenesis of UC, and huangqin tang can inhibit the relative activity of NF-κB p65, and decrease the expression levels of NO, IL-6, TNF-α and PGE2.

摘要

探讨黄芩汤对溃疡性结肠炎(UC)大鼠细胞因子表达及核因子-κB p65(NF-κB p65)的影响,并探究其潜在作用机制。采用复合造模法(三硝基苯磺酸和乙醇)制备具有细胞免疫反应性的UC大鼠模型。将大鼠随机分为对照组、模型组、柳氮磺胺吡啶(SASP)组以及黄芩汤高剂量组、中剂量组和低剂量组。治疗五天后,评估各组大鼠的进食量、体重及微观损伤情况。同时采集血液和结肠组织。采用Griess法检测一氧化氮(NO)的生成量,采用酶联免疫吸附测定法(ELISA)检测白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、前列腺素E2(PGE2)的表达水平。采用免疫组化法(ICH)检测结肠组织中NF-κB p65蛋白的表达。模型组大鼠的进食量和体重低于对照组。模型组血清中NO、IL-6、TNF-α、PGE2的表达水平及结肠组织中NF-κB p65蛋白高于对照组。黄芩汤高剂量组和中剂量组上述指标得到改善。但与SASP组相比无显著差异。NF-κB p65可能参与UC的发病机制,黄芩汤可抑制NF-κB p65的相对活性,降低NO、IL-6、TNF-α和PGE2的表达水平。

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