IGF-1对大鼠缺血、缺氧神经元p-JNK及p-P38表达的影响  

Influence of IGF-1 on p-JNK,p-P38 in hypoxia ischemia neurons of rat

作　　者：李智勇[1] 夏鹰[1] 陈晓东[1] 罗汉[1] 

机构地区：[1]海南省海口市人民医院神经外科,570208

出　　处：《重庆医学》2012年第16期1572-1574,F0003,共4页Chongqing medicine

摘　　要：目的研究胰岛素样生长因子-1(IGF-1)对缺血、缺氧大鼠脑皮质神经元凋亡的保护作用及作用机制。方法原代培养新生大鼠脑皮质神经元,建立缺血、缺氧细胞模型,观察IGF-1及IGF-1受体抑制剂(AG1024)对该模型细胞存活率(MTT试验)、细胞凋亡(流式细胞法)、JNK、P38表达(Western blot法)和Caspase-3活性(荧光测定法)的影响。结果 IGF-1(HII组)及AG1024(HIIA组)干预细胞模型24h后,模型细胞存活率分别为(77.00±3.80)%、(62.00±4.40)%;凋亡率分别达到14.58%、24.97%。IGF-1组可明显抑制p-JNK及p-P38的表达及Caspase-3的活性。结论 IGF-1对缺血、缺氧神经元损伤有一定的保护作用,并通过调控p-JNK、p-P38及Caspase-3的表达抑制缺血、缺氧神经元的凋亡。Objective To investigate the anti-apoptosis protective effects of insulin-like growth factor-1（IGF-1）on hypoxia is- chemia neurons of rats and its action mechanism. Methods Cortical neurons were cultured,and made hypoxia ischemia cell model. Hypoxia ischemia cells were incubated with IGF-lor AG1024 to study cell viability（MTT）, apoptosis（Flow cytometry）, JNK and P38 expression（Western blot） ,and Caspase-3 activation（fluorometric method）. Results Hypoxia ischemia cells were exposed to IGF-lor AG1024 for 24 h,and MTT assay showed that the ceil survival rates of IGF-I（HII group） and AG1024（HIIA group） were （77. 004-3.80） % and （62. 004-4.40） % ,respectively. The percentage of apoptotic cells was 14.58 % and 24.97 %, respectively. The expression of p-JNK,p-P38 and Caspase-3 activation were inhibited by IGF-1. Conclusion IGF-1 protects neurons against hy- poxia ischemia cells injure by inhibiting the expression of p-JNK,p-P38 and caspase-3 activation.

关 键 词：胰岛素样生长因子Ⅰ 缺氧缺血 脑神经元 JNK丝裂原活化蛋白激酶类 半胱氨酸天冬氨酸蛋白酶 

分 类 号：R714.7[医药卫生—妇产科学]