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.
出处
《重庆医学》
CAS
CSCD
北大核心
2012年第16期1572-1574,F0003,共4页
Chongqing medicine
