远志皂苷元抗H/R诱导皮层神经元凋亡的机制初探  

Preliminary mechanism of senegenin against H/R-induced apoptosis of primary cortical neurons

作　　者：赵严冬[1,2] 刘潘虹 李学敏[1,2] 鲁凡[3] 王华东[1,2] 陆大祥[1,2] 戚仁斌[1,2] 

机构地区：[1]暨南大学医学院病理生理学系 [2]国家中医药管理局病理生理实验室 [3]暨南大学附属第一医院骨科,广东广州510632

出　　处：《中国病理生理杂志》2014年第7期1166-1171,共6页Chinese Journal of Pathophysiology

基　　金：广州市科技计划(No.2014J4100098)

摘　　要：目的:初步探讨远志皂苷元(senegenin,Sen)对抗缺氧/复氧(hypoxia/reoxygenation,H/R)诱导大鼠原代皮层神经元凋亡的作用及机制。方法:提取原代大脑皮层神经元,培养至第6 d,进行相应的实验处理,分为正常对照组(control组)、模型组(H/R组)、Sen保护处理组(Sen+H/R组)和Sen处理组(Sen组)。流式细胞术检测各组凋亡率。采用Western blotting检测JNK、p-JNK、c-Jun、p-Jun、Bcl-2和Bax的表达变化。结果:H/R组与control组比较,细胞凋亡率显著升高(P<0.05);而H/R+Sen组细胞凋亡率显著低于H/R组(P<0.05),提示Sen可对抗H/R诱导的皮层神经元凋亡,模型构建成功;Westem blotting结果显示Sen可显著增强H/R模型中JNK和-c-Jun蛋白表达,抑制其磷酸化(P<0.05),上调Bcl-2蛋白表达并抑制Bax蛋白表达(P<0.05)。结论:Sen抗H/R诱导神经细胞凋亡,发挥保护作用的可能机制是通过上调JNK和c-Jun蛋白表达,并抑制其磷酸化,进而上调Bcl-2表达并抑制Bax表达等来实现的。AIM：To explore the preliminary mechanism of senegenin （ Sen） on inhibiting hypoxia/reoxygenation （ H/R）-induced apoptosis of primary cortical neurons .METHODS：The cultured cortical neurons were randomly divided in-to normal group （control group）, model group （H/R group）, Sen＋H/R group and Sen group.Flow cytometry was used to evaluate the effect of Sen on H/R-induced cell apoptosis .The protein levels of JNK , p-JNK, c-Jun, p-c-Jun, Bcl-2 and Bax were assessed by Western blotting .RESULTS：The apoptotic rate in H/R group was obviously higher than that in control group （P〈0.05）, while the apoptotic rate in Sen ＋H/R group was obviously lower than that in H/R group （P〈0.05）, suggesting that the model of apoptosis was established successfully .The results of Western blotting showed that Sen increased the expression of JNK and c-Jun, inhibited the phosphorylation of JNK and c-Jun （P〈0.05）, increased the protein level of Bcl-2 and inhibited the protein level of Bax in H/R treated primary cortical neurons （P〈0.05）.CONCLUSION：Sen has a protective effect against H/R-induced neuronal apoptosis by increasing the expression of JNK and c-Jun, inhibiting the phosphorylation of JNK and c-Jun, increasing the protein level of Bcl-2 and decreasing the protein level of Bax .

关 键 词：远志皂苷元 神经元 缺氧 复氧 细胞凋亡 

分 类 号：R363.2[医药卫生—病理学]