中文摘要：

目的 探讨高糖环境中肝X受体通过线粒体途径在调控H9C2细胞凋亡过程中的作用。方法 以H9C2细胞为研究对象,分为低糖组（Control组）、甘露醇组、高糖组、高糖＋T0901317组及高糖＋5CPPSS-50组。检测各组H9C2细胞的活性,细胞内活性氧水平,Bax、Bcl-2 m RNA,cleaved caspase-3蛋白的表达及细胞凋亡率,并观察细胞线粒体膜电位变化。结果 表达LXRs组明显降低高糖诱导的Bax m RNA、激活型caspase3蛋白表达和细胞内活性氧水平;上调高糖抑制的Bcl-2 m RNA表达和线粒体膜电位。结论 LXRs激动剂T0901317可改善高糖环境中H9C2细胞活性,抑制细胞凋亡,对细胞起到一定的保护作用;抑制LXRs后,对高糖环境中H9C2细胞损伤作用更明显。LXRs可通过线粒体途径调控高糖环境所致H9C2细胞凋亡。

英文摘要：

Objective To observe the viability and apoptosis level of H9C2 cells induced by high glucose and investigate the effect of liver X receptors（LXRs） on the regulation of apoptosis in H9C2 cells induced by high glucose through mitochondria-mediated pathway. Methods H9C2 cells were used in the experiments and divided into：low glucose group（control group） ;D-mannitol group;high glucose group;high glucose ＋T0901317 group and high glucose ＋5CPPSS-50 group. The viability and the level of ROS in the H9C2 cells were measured. The mRNA expressions of Bax and Bcl-2 were detected by qRT-PCR. The protein level of cleaved caspase 3 was determined by Western blot. The apoptotic rates of H9C2 ceils with different treatments were analyzed by cytometry with annexin V-FITC/PI double staining. Results Overexpressed LXRs significantly attenuated the mRNA expression of Bax induced by high glucose, cleaved caspase-3,cell viability and the ROS lever, and increased Bcl-2 expression and mitochondrial membrane potential inhibited by high glucose. Conclusions T0901317 improves the〉cell viability and reduces the apoptotic rate of H9C2 cells induced by high glucose,while inhibits the LXRs damage effect more obvious in H9C2 cells induced by high glucose. LXRs can regulate apoptosis in H9C2 cells induced by high glucose through mitoehondria-mediated pathway.