丁苯酞抑制原代大鼠海马神经元氧糖剥夺/复氧诱导的凋亡  

Neuroprotective effect of 3-n-butylphalide on injury induced by oxygen glucose deprivation/reoxygenation in primary neurons from rat hippocampus

作　　者：荣国铃[1] 吴世政[2] 张淑坤[3] 李娜[1] 于永才[2] 

机构地区：[1]青海大学医学院,西宁810007 [2]青海省人民医院神经内科,西宁810007 [3]青海省人民医院病理科,西宁810007

出　　处：《中国新药杂志》2011年第11期1015-1019,共5页Chinese Journal of New Drugs

基　　金：青海省医疗卫生领域人才小高地建设项目基金(2009-08)

摘　　要：目的:观察丁苯酞对氧糖剥夺/复氧(oxygen glucose deprivation/reoxygenation,OGD/R)诱导的SD大鼠原代培养海马神经元损伤的保护作用。方法:原代培养新生24 h内SD乳鼠海马神经元,建立氧糖剥夺30 min/复氧8 h海马神经元损伤模型。实验分为正常对照组、OGD/R模型组、丁苯酞低、中、高剂量组(0.1,1,10μmol·L-1)。采用Hoechest33258染色测定细胞凋亡,免疫细胞化学检测各组细胞中Bcl-2蛋白的表达情况。结果:与OGD/R模型组比较,各丁苯酞给药物组神经元凋亡率均不同程度降低(P<0.01),且随药物浓度升高而降低;Bcl-2蛋白表达不同程度地增高(P<0.01),且随药物浓度升高而升高。结论:丁苯酞能抑制OGD/R诱导的海马神经元细胞凋亡,其可能通过增加神经元内Bcl-2凋亡抑制蛋白的表达而抑制凋亡,进而保护神经元。To observe neuroprotective effect of 3-n-butylphalide （NBP） on injury induced by oxygen glucose deprivation/reoxygenation （OGD/R） , and investigate the possible mechanisms. Methods： Primary hippocampal neurons from newborn SD rats （ 〈 24 h） were cultured in vitro, and injury was induced by OGD/R （30 min/8 h）. Neurons were treated with NBP at O. 1, 1 and 10 Ixmol＇L6-1. Apoptotic cells were analyzed by Hoechest33258 staining. Bcl-2 expression was detected by immunocytochemistry. Results： Compared with OGD/R control, NBP significantly decreased neuronal apoptosis （P 〈0.01 ）, and increased the expression of Bcl-2 protein （P 〈 0.01） in a concentration-dependent manner. Conclusion： NBP inhibits OGD/R-induced apoptosis of hippocampal neurons and protecte the neurons. This effect may be via increasing apoptosis-inhibited Bcl-2 protein expression.

关 键 词：丁苯酞 海马神经元 氧糖剥夺/复氧 Bcl-2 凋亡 

分 类 号：R972[医药卫生—药品]