Neuroprotective Effects of 17β-Estradiol against Thrombin-Induced Apoptosis in Primary Cultured Cortical Neurons

被引:3
作者
Bao, Lei [1 ]
Zhou, Su [1 ]
Zhao, Hui [2 ]
Zu, Jie [1 ]
He, Qianqian [1 ]
Ye, Xinchun [1 ]
Cui, Guiyun [1 ]
机构
[1] Xuzhou Med Coll, Affiliated Hosp, Dept Neurol, Xuzhou 221004, Jiangsu, Peoples R China
[2] Xuzhou Cent Hosp, Dept Neurol, Xuzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
17; beta-estradiol; Intracerebral hemorrhage; Thrombin; JNK; Apoptosis; INDUCED BRAIN-DAMAGE; INTRACEREBRAL HEMORRHAGE; GLUCOSE DEPRIVATION; CEREBRAL-ISCHEMIA; SIGNALING PATHWAY; IN-VITRO; ESTROGEN; INJURY; RATS; OVEREXPRESSION;
D O I
10.1159/000440961
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
Aims: 17 beta-estradiol (E2) is a powerful neuroprotective agent in the central nervous system; however, little is known about its effects on intracerebral hemorrhage. This study examined the effects of E2 on thrombin-induced apoptosis in vitro and investigated the potential mechanisms. Methods: Primary cultured cortical neurons were treated with E2 or vehicle and then the cells were exposed to thrombin. Neuronal apoptosis was assessed by flow cytometry. The phosphorylated c-Jun-N-terminal kinase (p-JNK), phosphorylated extracellular signal-regulated kinases 1/2 (p-ERK1/2), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and caspase-3 were assayed by western blot. Results: Consequently, we found that E2 has significantly reduced the apoptosis in thrombin-treated neurons. E2 also exhibited a downregulation in the ratio of Bax/Bcl-2, caspase-3 and p-JNK. However, E2 had little effect on p-ERK1/2 proteins activation. Conclusion:Taken together, E2 has shown neuroprotective effects on thrombin-induced neuronal apoptosis, and the molecular mechanisms may correlate with the inhibition of the JNK signaling pathway. (C) 2015 S. Karger AG, Basel
引用
收藏
页码:284 / 289
页数:6
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