溃结灵对UC大鼠结肠黏膜pERK1/2、pMEK1/2蛋白水平的影响

目的观察溃结灵对TNBS法UC大鼠模型结肠黏膜pERK1/2、pMEK1/2蛋白水平的影响,并对其作用机制进行探讨。方法采用溃结灵对TNBS法UC大鼠模型进行治疗,治疗结束后采集结肠黏膜标本并提取全细胞蛋白,运用蛋白免疫印迹(Western blot)方法对PERK1/2和PMEK1/2的蛋白表达水平进行检测,以β-actin作为内参,以目的蛋白与β-actin密度的比值作为目的蛋白的相对含量,进行组间比较分析。结果模型组pERK1/2、pMEK1/2蛋白相对表达量分别是0.3974±0.1017和0.6994±0.1372,均高于正常组(分别为0.2037±0.1234、0.4092±0.1177,P0.05,P0.01);溃结灵组相对表达量分别为0.7060±0.1607和0.8928±0.1801,明显高于模型组(P0.01,P0.05);SASP组相对表达量分别为0.7299±0.2710和0.9053±0.1591,明显高于模型组(P0.01,P0.05)。结论溃结灵对TNBS法UC大鼠模型结肠黏膜pERK1/2、pMEK1/2蛋白表达有上调作用,提示溃结灵治疗作用可能与激活ERK信号转导途径有关。

Effect of Kuijieling Decoction on Protein Level of pMEK1/2 and pERK1/2 in Colonic Mucosa of Ulcerative Colitis Model Rats

Objective To observe the effect of Kuijieling Decoction (KD)on protein level of pMEK1/2 and pERK1/2 in colonic mucosa of rats with ulcerative colitis (UC )and to explore its possible mechanism. Methods Trinitro-ben-zene-sulfonic acid(TNBS)method was used for the establishment of UC rat model. After treatment with KD, the whole-cell protein was extracted from the colonic mucosa. Western blot technique was used to detect protein levels of pMEK1/2and pERK1/2. With β-actin as the internal index, relative expression of target protein was calculated from the gray scale ratio of target protein and β-actin. Results The results showed that relative protein expression of pERK1/2 was 0.3974±0.1017 and pMEK1/2 was 0.6994±0.1372 in the model group, higher than that in normal control group (0.2037±0.1234 and 0.4092±0.1177 respectively, P > 0.05, P < 0.01). Relative protein expression of pERK1/2 and pMEK1/2 in KD group was 0.7060±0.1607 and 0.8928±0.1801 respectively, significantly higher than that in the model group (P < 0.01, P < 0.05). Relative protein expression of pERK1/2 and pMEK1/2 in SASP group was 0.7299±0.2710 and 0.9053±0.1591, significantly higher than that in the model group (P < 0.01, P < 0.05). Conclusion: The relative protein expression of pMEK1/2 and pERK1/2 in colonic mucosa of UC model rats induced by TNBS is enhanced after treatment with KD, indicating that the therapeutic mechanism of KD in treating UC is probably related with the activation of ERK message transduction pathway.