中文摘要：

研究MPP^＋（1-methyl-4-phenylpyridinium）对PC12细胞的毒性作用及机制。采用MTT法检测细胞存活率,Western blotting检测蛋白变化及双荧光素酶报告基因系统检测转录因子活性。结果表明,MPP＋能够显著抑制细胞存活率,且呈剂量依赖性;而且MPP^＋能够降低PC12细胞神经营养因子BDNF（brain-derived neurotrophic factor）的蛋白水平,并能够抑制ERK（extracellular signal-regulated proteinkinase）的磷酸化,而对CaMKⅡ活性无影响,同时能够显著抑制BDNF的转录因子CREB（cAMP response element binding protein）的磷酸化,并抑制其转录活性。因此MPP＋可能通过抑制ERK活性而抑制其下游转录因子CREB的活性,最终导致BDNF的表达减弱。

英文摘要：

The aim of this study is to investigate the neurotoxic effect and mechanism of 1-methyl-4-pheny1-pyridinium （MPP^＋） on PC12 cells. MTT assay was used to investigate cell viability, Western blotting assay was performed to observe the protein level and phosphorylation, and dual-luciferase assay was used to study the transactivation. The experiment showed that MPP^＋ could decrease cell viability significantly in a dose-dependent manner and could decrease BDNF protein level, depress the phosphorylation of ERK, and attenuate the phosphorylation and transactivation of CREB, which is one of transcription factors of BDNF, but did not affect the activity of CaMK Ⅱ in PC12 cells. So MPP^＋ might decrease BDNF protein level through MAPK/ERK signal pathway.