【摘要】 目的:研究CysLTR1通路调节铝负荷肝细胞氧化应激及凋亡的作用机制。方法:HL-7702细胞用RPMI-1640培养，分为正常对照组、铝负荷组、MK-571+铝组，分别给予相应药物干预后，用MTT法检测细胞活力，确定CysLTR1抑制剂(MK-571)给药浓度。采用细胞流式技术检测各组细胞凋亡的情况，运用试剂盒检测各组细胞中的ALT、AST水平，SOD和MDA含量。运用WB技术测定各组细胞中Caspase3、Caspase9、Bcl-2和BAX的蛋白表达。结果:给予MK-571(3nmol/L)可以提高铝负荷L02细胞生存率(P<0.01),并降低铝负荷L02细胞凋亡指数(P<0.01),降低铝负荷细胞中ALT和AST水平(P<0.01),减少MDA的含量(P<0.01),同时提高SOD的活力(P<0.01)。MK-571还可以下调铝负荷细胞中Caspase3、Caspase9和BAX蛋白的表达(P<0.05和P<0.01),上调Bcl-2蛋白的表达(P<0.05)。结论:CysLTR1通路调节铝负荷肝细胞氧化应激，影响细胞凋亡机制，保护铝负荷肝细胞凋亡。更多还原

【Abstract】 Objective:To investigate the mechanism of the CysLTR1 signal pathway on oxidative stress and apoptosis of aluminum-loaded hepatocytes.Methods:HL-7702 cells were cultured in RPMI-1640 medium and divided into normal control group, aluminum loaded group and MK-571 group. Each group was given corresponding drug. Cell viability was detected by MTT assay to determine the concentration of MK-571. The apoptosis rate of each group was measured by flow cytometry(FCM), and the activities of ALT, AST, SOD, and MDA in the cells of each group were measured by the kits. The expressions of Caspase3, Caspase9, Bcl-2, and BAX proteins were measured by western blot assay. Results:The CysLTR1 inhibitor(MK-571; 3 nM, 36 hours) could validly enhance the survival rate(P<0.01), decreased the rate of apoptosis in aluminum-loaded L02 cells(P<0.01). The content of ALT, AST, and MDA were significantly decreased by treating with MK-571(P<0.01), and the activity of SOD was increased(P<0.01). Meanwhile, the expression of Caspase3, Caspase9, and BAX proteins were down-regulated significantly(P<0.05,P<0.01), and the level of Bcl-2 protein was up-regulated(P<0.05) treated with MK-571 in aluminum-loaded L02 cells. Conclusion:CysLTR1 pathway regulates oxidative stress, affects the apoptosis mechanism, and protects aluminum-loaded hepatocytes from apoptosis.更多还原