溃结灵对UC大鼠结肠黏膜pERK1/2、pMEK1/2蛋白水平的影响  

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

作　　者：宋宁[1] 李燕舞[1] 巫燕莉[1] 王汝俊[1] 

机构地区：[1]广州中医药大学脾胃研究所,广州510405

出　　处：《中药新药与临床药理》2010年第2期110-112,共3页Traditional Chinese Drug Research and Clinical Pharmacology

基　　金：国家自然科学基金项目(30772754);广东省中医药局课题(2007047)

摘　　要：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,P>0.05,P<0.01);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(P<0.01,P<0.05);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(P<0.01,P<0.05)。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。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-aetin as the internal index, relative expression of target protein was calculated from the gray scale ratio of target protein and β-aetin. 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 con- trol group （0.2037±0.1234 and 0.4092±0.1177 respectively, P 〉 0.05, P 〈 0.01）. Relative protein expression of pERK1/2 and pMEKI/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 proba- bly related with the activation of ERK message transduction pathway.

关 键 词：溃结灵 溃疡性结肠炎 大鼠模型 PERK1/2 pMEK1/2 

分 类 号：R285.5[医药卫生—中药学]