氧化应激性肠上皮细胞损伤与MAPK信号通路的关系研究  

The relationship between the injury-induced oxidative stress in intestinal epithelium cells and MAPK signaling pathways

作　　者：陈茜[1] 屠伟峰[2] 

机构地区：[1]南方医科大学附属广州军区广州总医院麻醉科,广东广州510010 [2]广州军区广州总医院麻醉科全军临床麻醉中心,广东广州510010

出　　处：《热带医学杂志》2011年第9期1004-1006,共3页Journal of Tropical Medicine

基　　金：江苏省高校省级重点实验室开放课题项目(KJS04001)

摘　　要：目的观察氧化应激引起肠上皮细胞(IEC-6)损伤后丝裂原活化蛋白激酶(MAPK)信号通路活化的情况,从而探讨氧化应激损伤的机制。方法采用MTT法检测不同浓度(100、200、300、400、500、800、1000、2000μmol/L)H2O2对IEC-6生存率的影响;用WesternBlot法检测H2O2作用不同时间(0.25、0.5、1、2、3、4h)下ERK、JNK以及p38磷酸化的激活情况。结果与正常组相比,随着H2O2刺激浓度的增加,IEC-6的生存率逐渐降低,呈浓度依赖性。当H2O2刺激浓度为200μmol/L时细胞的生存率约为50%。ERK1/2、JNK1/2、p38在H2O2刺激0.25h开始磷酸化,在刺激0.5h达到最高,随后磷酸化水平恢复到基础值。结论氧化应激早期可通过激活ERK、JNK以及p38的磷酸化引起IEC-6的损伤。Objective To determine the involvement of intracellular mitogen-activated protein kinase（MAPK） signaling transduction pathways in oxidative stress-induced intestinal epithelial cell injury. Methods MTT assay was used to measure the survival rate of H2O2-treated IEC-6 cells. Western Blot was used to detect the phosphorylation state of ERK, JNK and p38. Results ①Compared with the normal group, H2O2 dose-dependently increase the survival rate of IEC-6 cells. The survival rate of IEC-6 was approximately 50% when the concentration of H2O2 was 200 μmol/L. ②ERK,JNK and p38 began to be phosphorylated at 0.25 h and reached the highest level at 0.5 h, then back to the baseline value. Conclusion At the early stage of oxidative stress, phosphorylation activation of ERK, JNK and p38 may cause injury of IEC-6 cells.

关 键 词：氧化应激 肠上皮细胞 丝裂原活化蛋白激酶 

分 类 号：Q555.7[生物学—生物化学]