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目的:观察牛膝多肽(achyranthes bidentatapolypeptides,ABPP)对MPP~+(1-甲基-4-苯基-吡啶离子)损伤多巴胺能神经元的保护作用。方法:原代培养大鼠胚胎中脑多巴胺能神经元,与浓度50 ng/ml的ABPP或50ng/ml神经生长因子(NGF)共同孵育6 h,加入20μmol/L MPP~+损伤多巴胺能神经元12 h。使用四甲基偶氮唑盐(methyl thiaaolyl terazolium salt color imetry,MTT)比色法测定细胞活力;采用末端标记技术(Td T-mediated d UTP Nick-End Labeling,TUNEL)检测细胞凋亡;流式细胞仪检测细胞凋亡;Western Blot检测细胞凋亡相关蛋白Bcl-2和Bax的表达水平。结果:ABPP或NGF预处理6 h可增强多巴胺能神经元的细胞活力,抑制MPP~+损伤后多巴胺能神经元的凋亡,上调Bcl-2/Bax蛋白的表达水平。ABPP对大鼠多巴胺能神经元的保护作用优于NGF。结论:与NGF相比,ABPP发挥了更好的拮抗MPP~+对多巴胺能神经元损伤的作用,其机制可能与上调Bcl-2/Bax蛋白的表达水平相关。
AIM: To observe the protective effect of achyranthes bidentatapolypeptides (ABPP) on dopaminergic neurons injured by MPP ~ + (1-methyl-4-phenyl-pyridinium). Methods: Primary cultured rat embryonic midbrain dopaminergic neurons were incubated with ABPP or 50ng / ml NGF for 6 h at a concentration of 50 ng / ml. 20 μmol / L MPP ~ + -induced dopaminergic neurons 12 h. Cell viability was determined by MTT colorimetric assay. Apoptosis was detected by TdT-mediated dUTP Nick-End Labeling (TUNEL). Flow cytometry Cell apoptosis was detected by Western Blot. The expressions of Bcl-2 and Bax were detected by Western Blot. RESULTS: Pretreatment with ABPP or NGF for 6 h increased the viability of dopaminergic neurons, inhibited the apoptosis of dopaminergic neurons after MPP ~ + injury, and up-regulated the expression of Bcl-2 / Bax protein. ABPP protects rat dopaminergic neurons better than NGF. CONCLUSION: Compared with NGF, ABPP exerts a better antagonistic effect on dopaminergic neurons injury induced by MPP ~ +, which may be related to the up-regulation of Bcl-2 / Bax protein expression.