中文摘要：

很多研究显示出的背景那个氧化压力和 mitochondrial 参与是主要的在 neurodegenerative 疾病的发展触发因素。钴氯化物(CoCl_2 ) 在房间可以服务的 PC12 导致了房间死亡一在导致组织缺氧的 neuronal cytotoxicity 的 vitro 模型简单、方便。为了在导致了 cytotoxicity 和 mitochondrial 的 CoCl_2 上探索 geniposide 的效果，在老鼠 pheochromocytoma PC12 房间工作，我们在 apoptosis 相关的蛋白质的表达式上分析了 geniposide 的影响。方法 PC12 房间和 RNAi PC12 房间与 0 被对待， 12.5， 25， 50，为到为 12 个小时的 400 mol/L CoCl_2 的 12 个小时然后暴露的 100 mol/L geniposide。Bcl-2， Bax， P53 和 caspase-9 的房间生存能力，房间形态学，和表示用西方的弄污被决定。有 geniposide 的结果预告的处理显著地改进了房间生存能力和形态学，减少 Bax， P53 和 caspase-9 的表示，并且在 CoCl_2 质问的 PC12 房间增加了 Bcl-2 的表示。在 RNAi PC12 房间，然而， geniposide 没在这些蛋白质的表示上有重要效果。结论 Geniposide 保护 PC12 房间免受涉及 mitochondrial 的 CoCl_2 的伤害调停的 apoptosis，和 GLP-1 R 可能在 PC12 房间在 geniposide 的 neuroprotection 起一个关键作用。

英文摘要：

Background A number of studies have shown that oxidative stress and mitochondrial involvement are major triggering factors in the development of neurodegenerative diseases. Cobalt chloride （CoCl2）-induced cell death in PC12 cells may serve a simple and convenient in vitro model of hypoxia-induced neuronal cytotoxicity. To explore the effect of geniposide on COCl2 which induced cytotoxicity and mitochondrial function in rat pheochromocytoma PC12 cells, we analyzed the influence of geniposide on the expression of apoptosis-related proteins. Methods PC12 cells and RNAi PC12 cells were treated with 0, 12.5, 25, 50, 100 umol/L geniposide for 12 hours and then exposure to 400 umol/L COCI2 for 12 hours. Cell viability, cell morphology, and expression of Bcl-2, Bax, P53 and caspase-9 were determined using Western blotting. Results Pretreatment with geniposide markedly improved the cells viability and morphology, decreased the expression of Bax, P53 and caspase-9, and increased the expression of Bcl-2 in PC12 cells challenged by CoCl2. However, in the RNAi PC12 cells, geniposide had no significant effect on the expression of these proteins. Conclusion Geniposide protects PC12 cells from CoOl2 involved in mitochondrial mediated apoptosis, and GLP-1R might play a critical role in the neuroprotection of geniposide in PC12 cells.