摘要
目的研究越鞠丸醇提物(YJ-E)对1-甲基-4-苯基-1,2,3,6-四氢吡啶离子(MPP+)所致大鼠嗜铬细胞(PC12)损伤的保护作用,并探讨其作用机制。方法 PC12细胞给予1 mmol/L MPP+,制备帕金森病(PD)离体模型。应用四甲基偶氮唑盐(MTT)法检测细胞活力,Hoechst染色法观察细胞凋亡,观察YJ-E对PC12细胞的保护作用。应用Western blotting检测垂体腺苷酸环化酶激活肽(PACAP)的表达及细胞外调节蛋白激酶(ERK)、环磷腺苷效应元件结合蛋白(CREB)的磷酸化水平。结果 3个浓度1.0、2.0、4.0 mg/m L的YJ-E均能显著改善MPP+模型中PC12细胞的存活(P<0.01),而对正常PC12细胞的存活无显著影响(P>0.05)。同时YJ-E可显著上调MPP+模型中PC12细胞PACAP的表达(P<0.01),并且显著上调ERK、CREB的磷酸化(P<0.01)。结论 YJ-E对MPP+模型中的PC12细胞具有保护作用,其机制可能是通过上调PACAP的表达及其下游ERK、CREB的磷酸化。
OBJECTIVE To investigate the neuroprotective effect and the mechanism of Yueju alcohol extract（ YJ-E） on chromaffin cells（ PC12） injury in rats induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine ion（ MPP＋）. METHODS PC12 cells were given 1 mmol MPP＋to establish Parkinson＇s disease（ PD） model in vitro. The protective effects of YJ-E on PC12 cells were measured by MTT assay and Hoechst staining. The expression of pituitary adenylate cyclase activating polypeptide（ PACAP） and the phosphorylation of extracellular regulated kinase（ ERK） and c AMP response element binding protein（ CREB） were determined by Western blotting. RESULTS YJ-E（ 1. 0, 2. 0, 4. 0 mg / m L） improved the survival of MPP＋-injured PC12 cells significantly（ P〈0. 01）, and displayed no significant effect on normal PC12 cells（ P〉0. 05）. Meanwhile, YJ-E up-regulated the expression of PACAP and the phosphorylation of ERK and CREB significantly（ P〈0. 01） of MPP＋-injured PC12 cells. CONCLUSION YJ-E shows promising neuroprotective effects on PC12 cells in MPP＋-induced Parkinson＇s disease model, and the mechanism may be associated with the up-regulation of the expression of PACAP and the phosphorylation of downstream ERK and CREB.
出处
《南京中医药大学学报》
CAS
CSCD
北大核心
2015年第2期156-159,共4页
Journal of Nanjing University of Traditional Chinese Medicine
基金
南京中医药大学青年自然科学基金(12XZR03)
江苏省中医药管理局资助项目(LZ11113)
