Naringin Protects H9c2 Cardiac Cells Against High Glucose-induced Injury by Inhibiting STAT3 Pathway

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.