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目的:研究六棱菊总黄酮(LAF)对溃疡性结肠炎(UC)大鼠模型的作用及其可能的分子生物学机制。方法:采用三硝基苯磺酸(TNBS)塑造UC大鼠模型,并予以不同剂量的LAF进行干预,用HE染色病理学检侧LAF对UC的疗效,用FCM检测LAF对大鼠UC模型结肠黏膜上皮细胞的凋亡率,用DNA琼脂糖电泳检测结肠黏膜细胞凋亡的生化特征,用western blot检测结肠黏膜细胞Bcl-2、Bax、Cyt-c、Caspase-9、Caspase-3蛋白表达情况。结果:LAF对UC大鼠模型有着显著的疗效,经不同浓度的LAF作用结肠黏膜细胞后,与模型组比较,细胞凋亡数目减少,组间有统计学意义(P<0.05),琼脂糖电泳DNA典型的梯形条带消失,伴随Bcl-2蛋白表达上调,Cyt-c、Caspase-9、Caspase-3蛋白表达下调(P<0.05),Bax蛋白表达无明显变化(P>0.05),而Bcl-2/Bax比值下降(P<0.05)。结论:LAF对UC大鼠模型有着显著的疗效,其机制可能通过线粒体凋亡途径抑制凋亡相关。
Objective: To study the effect of total flavonoids of Ligusticum chuanxiong (LAF) on rat model of ulcerative colitis (UC) and its possible molecular biological mechanism. Methods: The rat model of UC was established by trinitrobenzene sulfonic acid (TNBS). The rats were treated with different doses of LAF. The curative effect of LAF on UC was examined by HE staining. The effect of LAF on the colon The apoptosis rate of mucosal epithelial cells was detected by DNA agarose gel electrophoresis. The protein expression of Bcl-2, Bax, Cyt-c, Caspase-9 and Caspase-3 in colonic mucosal cells was detected by western blot . Results: LAF had a significant therapeutic effect on UC rat model. After treated with different concentrations of LAF, the number of apoptotic cells in the colon mucosa decreased compared with the model group (P <0.05) The expression of Bcl-2, Caspase-9 and Caspase-3 were down-regulated (P <0.05), while the expression of Bax was no significant change (P> 0.05) -2 / Bax ratio decreased (P <0.05). Conclusion: LAF has a significant effect on UC rat model, and its mechanism may inhibit apoptosis through mitochondrial apoptosis pathway.