中文摘要：

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。

英文摘要：

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.