【摘要】 目的探讨柚皮苷是否通过抑制信号转导子和转录激活子3(STAT3)通路保护H9c2心肌细胞对抗高糖引起的损伤。方法应用35 mmol/L的高浓度葡萄糖(高糖,HG)处理H9c2心肌细胞24 h,建立HG损伤心肌细胞模型;细胞计数试剂盒8测定细胞存活率;Hoechst 33258核染色荧光显微镜照相法测定细胞凋亡;双氯荧光素染色/荧光显微镜照相法测定胞内活性氧(ROS)水平;罗丹明123染色法测定线粒体膜电位(MMP);Western blot法测定STAT3蛋白表达水平。结果 HG处理H9c2心肌细胞24 h能引起明显的损伤,使细胞存活率降低,凋亡细胞数量和胞内ROS生成增多,MMP丢失;HG能增加STAT3磷酸化水平;柚皮苷预处理能明显抑制HG上调STAT3磷酸化水平这一作用;柚皮苷和STAT3通路抑制剂AG490能阻断HG对心肌细胞的上述损伤作用,包括细胞毒性、凋亡、ROS生成增多及MMP丢失等。结论柚皮苷可通过抑制STAT3通路保护H9c2心肌细胞对抗高糖引起的损伤。更多还原

【Abstract】 Aim To explore whether naringin( NRG) protects H9c2 cardiac cells against high glucose( HG)-induced injury by inhibition of signal transducers and activators of transcription 3( STAT3) pathway. Methods H9c2 cardiac cells were treated with 35 mmol / L glucose( HG) for 24 h to establish a model of HG-induced injury; Cell counter kit-8( CCK-8) was used to measure cell viability; Apoptotic cells were tested by Hoechst 33258 nuclear staining followed by fluorescence imaging; Intracellular levels of reactive oxygen species( ROS) were detected by 2’,7’-dichlorfluoresceindiacetate( DCFH-DA) staining,followed by fluorescence imaging; Mitochondrial membrane potential( MMP) was measured by a fluorescent dye,rhodamine 123( Rh123),followed by fluorescence imaging; The expression levels of STAT3 protein were detected by Western blot assay. Results Treatment of H9c2 cardiac cells with HG for 24 h significantly induced injuries,evidenced by a decrease in cell viability,increases in amount of apoptotic cells and intracellular ROS production,as well as a loss of MMP; HG enhanced the expression of phosphorylated( p)-STAT3; Pretreatment with NRG markedly inhibited the up-regulation of expression of p-STAT3 induced by HG; Pretreatment with NRG or AG490,an inhibitor of STAT3 pathway,attenuated the above HG-induced injuries,including cytotoxicity,apoptosis,increase in ROS production and a loss of MMP,in H9c2 cardiac cells. Conclusion NRG may protect H9c2 cardiac cells against the HG-induced injuries by inhibiting the STAT3 pathway.更多还原