梓醇对氧糖剥夺诱导PC12细胞凋亡的保护作用  

Catalpol Protects Rats' Pheochromocytoma Cells Against Oxygen-glucose Deprivation-induced Injury

作　　者：汪卓[1] 安利佳[1] 段延龙[1] 李亚晨[1] 姜波[1] 

机构地区：[1]大连理工大学生物科学与工程系,大连116024

出　　处：《现代生物医学进展》2006年第12期31-33,共3页Progress in Modern Biomedicine

摘　　要：目的:观察梓醇对氧糖剥夺(OGD)诱导PC12细胞凋亡的保护作用。方法:采用Hoechst 33258 DNA染色法,四甲基偶氮唑盐(MTT)检测细胞活性;化学比色法测定乳酸脱氢酶(LDH)的释放量,用流式细胞技术检测细胞凋亡比例以及P53和Bcl-2蛋白。结果:OGD可导致PC12细胞活力明显下降,LDH释放量增加、P53蛋白表达上升,Bcl-2蛋白表达下降。梓醇可明显改善细胞形态结构,显著降低LDH释放量、降低P53蛋白的表达,提高Bcl-2蛋白的表达,降低细胞凋亡率。结论:梓醇通过调节细胞凋亡相关基因的表达而抑制细胞凋亡。Objective： To investigate the effect of catalpol in apoptosis in PC12 cells induced by oxygen-glucose deprivation （OGD）. Methods： The morphological changes were observed by Hoechst 33258 staining assay; the cell viability was analyzed by MTT; the apoptosis rate, the protein of P53 and Bd-2 were measured by flow cytometry analysis （FCM）. Results： OGD could result in the decrease of cell viability, the increase of release of LDH, the dropping of Bcl-2 protein expression of PC12 cell, the rising of P53 protein expression of PC12 cell. Catalpol could improve the morphology of cells. It could increase bcl-2 protein expression, decrease P53 protein expression and the release of LDH, and reduce apoptotic rate. Conclusion： Catalpol could inhibit PC12 cells apoptosis by regulating related genes of apoptosis.

关 键 词：梓醇 PC12细胞 细胞凋亡 基因 

分 类 号：R743.3[医药卫生—神经病学与精神病学] R285.6[医药卫生—临床医学]