杜鹃兰乙醇提取物对谷氨酸诱导的PC12细胞损伤的保护作用

Neuroprotection effect of the extract of Cremastra appendiculata (D. Don) Makino against glutamate-induced PC12 cells injury and its possible mechanism

目的:研究杜娟兰乙醇提取物(CAME)对谷氨酸诱导的PC12细胞损伤的保护作用并且初步探讨其机制。方法:建立谷氨酸诱导的PC12细胞损伤的模型,预给予不同浓度的CAME处理细胞,检测细胞存活率、乳酸脱氢酶(LDH)、胞内活性氧(ROS)、超氧化物歧化酶(SOD)、丙二醛(MDA)和凋亡蛋白Bax,Bcl-2和caspase-3的表达量。结果:与造模组相比,CAME呈剂量依赖性提高谷氨酸诱导的损伤PC12细胞的细胞存活率,降低LDH释放量和胞内ROS生成量,提高SOD酶活力,减少MDA含量,抑制caspase凋亡级联反应。结论:CAME能够显著减少PC12细胞内由于氧化应激而产生过多的ROS,进而通过抑制线粒体凋亡途径而发挥其神经保护的作用。

Objective： To determine the neuroprotection effect of the extract of Cremastra appendiculata（D. Don） Makino against glutamate-induced PC12 cells injury and the possible mechanism. Methods： A model of glutamate-induced PC12 cells injury was established,and the cell viability,the release of lactate dehydrogenase（LDH）,the production of reactive oxygen species（ROS）,the levels of superoxide dismutase（SOD） and malonaldehyde（MDA）,and the expression of apoptosis protein were investigated. Results： Compared with the glutamate group,the cell viability was increased as well as the levels of SOD in CAME-pretreated groups in dose-dependent manner. On the contrary,the release of LDH and the production of ROS and MDA were decreased significantly,and the caspase cascade reaction was also inhibited. Conclusion： Overproduction of ROS caused by oxidative stress in PC12 cells can be scavenged by CAME effectively via inhibiting the mitochondria apoptosis pathway.