阿利吉伦对糖氧剥夺损伤SH-SY5Y细胞的保护机制  

Protective Mechanisms of Aliskiren on Damage of SH-SY5Y Cells Induced by Oxygen-Glucose Deprivation

作　　者：陆婉杏[1,2] 蒙兰青[1] 黄晓华[1] LU Wanxing;MENG Lanqing;HUANG Xiaohua(Department of Neurology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi Zhuang Autonomous Region, 533000, China;Department of Neurology, Minzu Hospital of Guangxi Zhuang Autonomous Region, Nannian, 530000, China)

机构地区：[1]右江民族医学院附属医院神经内科,广西壮族自治区白色市533000 [2]广西壮族自治区民族医院神经内科,南宁市530000

出　　处：《医学分子生物学杂志》2019年第3期258-262,268,共6页Journal of Medical Molecular Biology

基　　金：2014年度广西高校科学技术研究项目(No.YB2014301).

摘　　要：目的研究阿利吉仑(Aliskiren)对糖氧剥夺(oxygen-glucose deprivation, OGD)损伤的神经母细胞瘤细胞SH-SY5Y的保护机制。方法将SH-SY5Y细胞随机分成正常组[不作糖氧剥夺(oxygen-glucose deprivation, OGD)处理],OGD 组和阿利吉仑低、中、高剂量组(5.0, 10.0, 20. 0μmol/L),除了正常组,其余4组均OGD处理4h,流式细胞仪检测细胞凋亡;RT-PCR检测MKT、ERK和MTOR相应mRNA表达水平;Western印迹检测p-AKT^Thr308、p-AKT^Ser473、p-ERK1/2和p-MTOR蛋白表达水平。结果与OGD组相比,阿利吉仑组的细胞凋亡率呈剂量依赖性降低。RT-PCR和Western印迹检测结果表明:与正常组相比,OGD组的AKT、ERK和MTOR相应mRNA及磷酸化蛋白表达水平更低(P<0.05)。与OGD组比较,阿利吉仑组的AKT、ERA和MTOR相应mRNA及磷酸化蛋白表达水平呈剂量依赖性升高(P<0.05)。结论ERK1/2和PI3K/AKT/MTOR信号通路的激活可能是阿利吉仑对OGD损伤的SH-SY5Y细胞发挥保护作用的重要分子机制。Objective To investigate the protective mechanisms of Aliskiren on oxygen-glucose deprivation (OGD)-induced injury in SH-SY5Y cells. Methods SH-SY5Y cells were randomly divided into normal group, in which the cells were cultured in the absence of OGD treatment, OGD group and Aliskiren groups, in which cells were subjected to OGD for 4 h and given treatment of different concentrations of Aliskiren (5. 0, 10. 0, 20. 0μmol/L) or not. The apoptosis rate of SH-SY5Y cells was detected by flow cytometry. The mRNA levels of AKT, ERK1/2 and MTOR were measured by RT-PCR assay. The expressions of p-AKT^Thr308 , p-AKT^Ser473 , p-ERK1/2 and p-MTOR were detected by Western blotting. Results The apoptosis rate of SH-SY5Y cells was dose-dependently decreased in Aliskiren groups as compared with that in OGD group. RT-PCR and Western blotting showed that the mRNA and protein levels of AKT^Thr308, AKT^Ser473, ERK1/2 and MTORof SHSY5Y cells were significantly decreased in OGD group when compared with those in normal group (P <0. 05 ). However, they were significantly increased in Aliskiren groups (P <0. 05 ). Conclusion The protective mechanisms of Aliskiren on SH-SY5Y cells after OGD injury may be related to the activation of ERK1/2 and PI3 K/AKT/MTOR signaling pathways.

关 键 词：阿利吉仑 SH-SY5Y细胞 糖氧剥夺损伤 ERK1/2信号通路 PI3K/AKT/MTOR信号通路 

分 类 号：R743.3[医药卫生—神经病学与精神病学]