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目的:观察溃疡性结肠炎(UC)模型大鼠结肠黏膜固有层淋巴细胞凋亡及其凋亡调控蛋白Fas、FasL的表达以及清肠栓对相关表达的影响,探讨清肠栓治疗溃疡性结肠炎的作用机制。方法:用5%2,4,6-三硝基苯磺酸100mg/kg灌肠建立大鼠UC模型,运用电镜、原位末端标记细胞凋亡检测法(TUNEL法)和Fas、FasL蛋白免疫组化染色法,分别检测正常大鼠、UC模型大鼠以及经柳氮磺胺吡啶或清肠栓治疗后的大鼠结肠黏膜固有层淋巴细胞凋亡及固有层淋巴细胞Fas、FasL蛋白的表达情况。结果:与正常组相比,模型组大鼠结肠黏膜固有层淋巴细胞凋亡减慢,结肠黏膜固有层淋巴细胞上FasL的表达率增加,Fas的表达率下降。经清肠栓治疗后UC模型大鼠淋巴细胞凋亡增加,结肠黏膜固有层淋巴细胞上FasL的表达率下降,Fas的表达率增加。结论:溃疡性结肠炎的发病可能是由于结肠黏膜固有层FasL高表达与Fas表达不同步,降低了Fas/FasL介导的淋巴细胞凋亡率,导致淋巴细胞凋亡减慢。清肠栓可能因为诱导结肠黏膜固有层FasL与Fas同步表达,诱导结肠黏膜固有层淋巴细胞凋亡,从而达到缓解溃疡性结肠炎的目的。
Objective: To observe the apoptosis of lymphocytes in the colonic mucosa of ulcerative colitis (UC) rats and the expression of Fas and FasL, and the effect of Qingchang suppository on the expression of Fas and FasL. The mechanism of action of inflammation. METHODS: Rat UC models were established by enema with 5% 2,4,6-trinitrobenzene sulfonic acid (100 mg/kg), electron microscopy, in situ end labeling (TUNEL) and Fas and FasL protein immunization groups. By staining, we detected the apoptosis of lymphocytes in the colonic mucosa and the expression of Fas and FasL proteins in lamina propria in normal rats, UC model rats, and rats treated with sulfasalazine or Qingchang suppository. RESULTS: Compared with the normal group, the apoptosis of colonic lamina propria lymphocytes in the model group was slowed down, the expression rate of FasL on the lamina propria lymphocytes in the colonic mucosa increased, and the Fas expression rate decreased. After clear bowel suppository treatment, the apoptosis of lymphocytes increased in UC model rats, and the expression rate of FasL on lymphocytes in the colonic lamina propria decreased, and the expression rate of Fas increased. Conclusions: The onset of ulcerative colitis may be due to the high expression of FasL in the colonic lamina propria and the lack of Fas expression, which reduces the lymphocyte apoptosis rate mediated by Fas/FasL and leads to a decrease in lymphocyte apoptosis. Qingchang suppository may be induced by the simultaneous expression of FasL and Fas in the colonic mucosal lamina propria, which induces lymphocyte apoptosis in the lamina propria of the colonic mucosa, thereby achieving the goal of relieving ulcerative colitis.