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’-dichlorfluorescein-diacetate （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.