TLR4参与缺血后处理对缺血再灌注损伤致细胞凋亡的保护作用  

TLR4-mediated protective effect by brain ischemia postconditioning against apoptosis

作　　者：刘军[1] 毛善平[1] 董慧敏[1] 赵海专[2] 邢变枝[3] 郭晓洁[1] 

机构地区：[1]武汉大学人民医院神经内科,研究生430060 [2]武汉大学人民医院医疗部,430060 [3]武汉大学人民医院放射科,430060

出　　处：《卒中与神经疾病》2014年第3期144-147,161,共5页Stroke and Nervous Diseases

基　　金：武汉市科技攻关计划项目(2013060602010270)

摘　　要：目的探讨TLR4是否参与缺血后处理对PC12细胞缺血再灌注损伤致细胞凋亡的保护作用及其作用机制。方法将PC12细胞分为4组:正常组、缺血再灌注组、缺血后处理组及缺血后处理+脂多糖组,通过流式细胞术Annexin-FITC和PI双染法检测各组PC12细胞凋亡率,Western blotting检测各组细胞TLR4及Caspase-3表达水平,通过RT-PCR测定各组TLR4mRNA水平。结果缺血后处理可以降低缺血再灌注组细胞TLR4蛋白表达、mRNA水平及凋亡率,脂多糖可以逆转其下降趋势。结论 TLR4可能参与了缺血后处理对PC12细胞缺血再灌注损伤致细胞凋亡的保护作用。Objective To investigate whether TLR4 is involved in the protective effect of brain ischemia postconditioning against apoptosis. Methods The PC12 cells were divided into 4 groups： the control group, the ischemia/reperfusion group, the ischemic postconditioning group, the ischemic postconditioning/Lipopolysaceharides group. Apoptosis rate was detected by flow cytometry Annexin-FITC and PI double staining. Reverse transcription-PCR（RT-PCR）and western blot were used to observe the expression of TLR4 and cleaved caspase-3. Results Ischemia postconditioning could reduce TLR4 protein expression, mRNA level and apop- tosis rate of ischemia-reperfusion group, and LPS can reverse its downward trend. Conclusions TLR4 is involved in the protective effect by brain ischemia postconditioning against apoptosis.

关 键 词：缺血后处理 PC12细胞 TLR4凋亡 

分 类 号：R743[医药卫生—神经病学与精神病学]