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目的:观察溃结灵对TNBS法UC大鼠模型结肠粘膜pMEK1/2、pERK1/2蛋白水平的影响。方法:UC大鼠模型采用TNBS法,提取结肠粘膜全细胞蛋白,运用蛋白免疫印迹(Western blot)方法对pMEK1/2和pERK1/2的蛋白表达水平进行检测。结果:与正常组比较,3d时模型组pMEK1/2、pERK1/2蛋白相对含量略有升高,7d时pMEK1/2、pERK1/2均持续增高,14d时pMEK1/2、pERK1/2均明显增高。与模型组比较,3d时溃结灵组和SASP组pMEK1/2,pERK1/2蛋白相对含量均略有增高,7d时溃结灵组及SASP组pMEK1/2、pERK1/2均持续增高(P<0.05,P<0.01,P<0.05),14d时溃结灵组及SASP组均明显高于模型组(P<0.05,P<0.01)。结论:溃结灵对TNBS法UC大鼠模型结肠粘膜pMEK1/2、pERK1/2蛋白表达有上调作用,提示MEK/ERK信号通路可能是溃结灵修复UC大鼠模型肠道损伤粘膜的途径之一。
Objective: To observe the effect of Kuijieling on the protein level of pMEK1 / 2 and pERK1 / 2 in colonic mucosa of UC rats induced by TNBS. Methods: The UC rat model was used to extract the whole cell mucosal protein of TNM, and the protein expression level of pMEK1 / 2 and pERK1 / 2 were detected by Western blot. Results: Compared with normal group, the relative content of pMEK1 / 2 and pERK1 / 2 in model group increased slightly at 3d, pMEK1 / 2 and pERK1 / 2 increased at 7d, pMEK1 / 2 and pERK1 / 2 increased significantly at 14d Increase. Compared with the model group, the relative contents of pMEK1 / 2 and pERK1 / 2 protein increased slightly in KD group and SASP group on 3d, and pMEK1 / 2 and pERK1 / 2 increased in KD group and SASP group on the 7th day (P <0.05, P <0.01, P <0.05). On the 14th day, the rats in Kuijieling group and SASP group were significantly higher than those in model group (P <0.05, P <0.01). Conclusion: Kuijieling can up-regulate the expression of pMEK1 / 2 and pERK1 / 2 in the colon mucosa of UC rats induced by TNBS, suggesting that the MEK / ERK signal pathway may be the route of UCJ injury in mucosa of UC rats one.