曲古抑菌素A对缺糖/缺氧损伤PC12细胞的保护作用  

Protective effect of TSA on PC12 cell injury induced by the deprivation of oxygen/glucose

作　　者：越茂松[1] 黄琼[1] 王进京[1] 季秋虹[2] 季煜华[1,3] 

机构地区：[1]暨南大学生命科学技术学院组织移植与免疫研究中心,广州510632 [2]南通大学附属医院神经内科,南通226001 [3]暨南大学功能蛋白质研究广东普通高校重点实验室,广州510632

出　　处：《中国药理学通报》2013年第5期688-692,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金(No 30900563;81071483;81201016;81272027);中央高校基本科研业务费专项资金项目;江苏省教育厅自然科学基金项目(No 10KJB180006)资助

摘　　要：目的研究组蛋白去乙酰化酶抑制剂曲古抑菌素A(trichostatin A,TSA)对PC12大鼠肾上腺嗜铬细胞瘤细胞缺糖/缺氧损伤的保护作用及其可能的作用机制。方法建立PC12细胞缺糖/缺氧(oxygen and glucose deprivation,OGD)损伤模型,1-640 nmol.L-1TSA处理细胞,噻唑蓝(MTT)检测对PC12细胞活性的影响,Propidium iodide(PI)和Hoechst33258染色检测细胞凋亡与坏死,荧光显微镜和流式细胞仪检测各组细胞内活性氧(ROS)的含量。结果与模型组相比,80 nmol.L-1TSA可明显提高ODG PC12的细胞存活率,降低细胞内的ROS含量(P<0.05)。结论 TSA对OGD损伤的PC12细胞具有保护作用,其机制可能是通过增加细胞内能量代谢中各种酶的乙酰化水平来应对缺血损伤。Aim To study the protective effects of histone deacetylase inhibitor （HDACi） , trichostatin A （TSA）, on oxygen/glucose deprivation （OGD） injuried PC12 cells and its underlying mechanism. Methods PC12 OGD injury model was established by using cobalt chloride （ CoCl2 ） and glucose-free medium , and treated by 1-040 nmol.L-1 TSA. Cell viability was measured by MTT assay, cell apoptosis and necrosis was observed by PI and Hoechst staining, and flow cytometry detection and fluorescence microscope were applied to determine the reactive oxygen species in each group. Results Compared with control group, 80 nmol.L-1 TSA significantly improved cell viability and reduced intracellular reactive oxygen species （ROS）. Conclusions TSA protects the OGD injured PC12 ceils. The possible underlying mechanisms may be related to maintaining or increasing the acetylation level of the energy metabolism enzymes, whereby keeping the PC12 cells from the injury induced by OGD.

关 键 词：TSA PC12细胞 缺糖 缺氧 能量代谢 乙酰化 活性氧 

分 类 号：R-332[医药卫生] R329.24