摘要
目的观察甲基苯丙胺(Meth)通过电压门控钾离子通道亚型1.3、1.5(Kv1.3、Kv1.5)对大鼠胎鼠小胶质细胞的损伤作用。方法 SD胎鼠原代培养小胶质细胞,细胞计数试剂盒(CCK-8)检测细胞活力和原位末端转移酶标记技术(TUNEL)检测细胞凋亡;采用蛋白质印迹法和实时荧光定量聚合酶链反应法观察Kv1.3、Kv1.5表达变化。结果 Meth呈浓度依赖性降低小胶质细胞活力,增加小胶质细胞凋亡;Kv1.3的抑制剂MgTx对Meth所致小胶质细胞损伤有部分保护作用;与对照组(1.047±0.165)比较,300μmol/L Meth组小胶质细胞Kv1.3 mRNA表达(7.453±0.675)增高(P<0.05),MgTx组Kv1.3 mRNA表达(1.684±0.875)低于Meth 300μmol/L组(P<0.05);Meth对Kv1.5 mRNA表达无影响。结论 Meth可引起小胶质细胞损伤,其机制可能与Kv1.3表达变化有关。
Objective To investigate the effect of methamphetamine（Meth） on the expression of voltage-gated potassium channel subtype 1.3 and 1.5（Kv1.3 and Kv1.5） with primary cultured fetal rat cortical microglia.Methods The cell viability and apoptosis were detected with CCK-8 as well as terminal deoxyribonucleotidyl transferase（TdT）-mediated biotin-16-dUTP nick-end labeling（TUNEL） assay.The expression of Kv1.3 and Kv1.5 mediated by Meth was evaluated with real-time PCR and western blot.Results Meth reduced cell viability and increased cell apoptosis in a dose-dependent manner.Compared with that of the control（1.047±0.165）,Meth could increase the mRNA expression of Kv1.3（7.453±0.675）.But this process could be partly retarded by MgTx（1.684±0.875）.The mRNA expression of Kv1.3,but not Kv1.5,was up-regulated by Meth.Conclusion Kv1.3 is involved in Meth mediated microglia cell injury.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2013年第6期820-822,共3页
Chinese Journal of Public Health
基金
国家自然科学基金青年基金(81202230)
国家自然科学基金(81273115)
江苏省高校优势学科建设工程项目(CX09B_264Z)
南京医科大学科技发展基金重点项目(2011NJMU275)
