Prdx6在缺血缺氧状态下对肝细胞的保护作用及其机制

发布时间：2018-07-09 20:14

本文选题：过氧化物氧化还原酶 + 活性氧　；参考：《广东医学》2017年20期

【摘要】：目的探讨Prdx6在缺血缺氧状态下对肝细胞的保护作用及其机制。方法将L02细胞在缺血缺氧状态下分别培养6、12、18 h和24 h,收集细胞培养基检测其中的ALT、AST和LDH,使用ROS检测试剂盒检测细胞内ROS水平,CCK8试剂盒检测细胞活力,流式细胞仪检测L02细胞的凋亡,Western blot检测细胞中Prdx6蛋白及IκB、pIκB蛋白的表达变化;构建pI RES2-ZsG reen1-Prdx6质粒转染L02细胞过表达Prdx6,再次检测Prdx6蛋白的表达、细胞的损伤情况及细胞内ROS水平。结果缺血缺氧状态下细胞培养基内ALT、AST和LDH上升,细胞内ROS水平上升,细胞凋亡增加,细胞活力下降,Prdx6蛋白表达下降,NF-κB相关蛋白IκB表达下降、pIκB表达上升,且其变化程度随着缺血缺氧时间的延长而更明显。过表达Prdx6可以降低细胞内ROS水平,减轻细胞的缺血缺氧性损伤。结论 Prdx6蛋白在缺血缺氧状态下可通过降低细胞内ROS水平,减轻细胞损伤,发挥对细胞的保护作用。
[Abstract]:Objective to investigate the protective effect and mechanism of Prdx6 on hepatocytes under ischemia and hypoxia. Methods L02 cells were cultured under ischemia and hypoxia for 18 h and 24 h, respectively. ALTX AST and LDH were detected in cell culture medium. Ros assay kit was used to detect intracellular Ros level and CCK8 assay kit was used to detect the viability of L02 cells. The expression of Prdx6 protein and I 魏 B pI 魏 B protein in L02 cells was detected by flow cytometry, and the pIRES2-ZsG reen1-Prdx6 plasmid was constructed and transfected into L02 cells to detect the expression of Prdx6 protein, cell damage and intracellular Ros level. Results under the condition of ischemia and hypoxia, ALT AST and LDH increased, Ros level increased, apoptosis increased, cell viability decreased and Prdx6 protein expression decreased. The expression of NF- 魏 B related protein I 魏 B decreased and the expression of Pi 魏 B increased. And its change degree is more obvious with the prolongation of the time of ischemia and hypoxia. Overexpression of Prdx6 can reduce the level of Ros and reduce the ischemic and hypoxic injury. Conclusion Prdx6 protein can protect cells by reducing Ros level and cell injury.
【作者单位】：武汉市普爱医院(西院)急诊外科;
【分类号】：R575

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