Abstract:Objective To investigate the change in chloride ion (Cl-) concentration in high glucose-induced cardiomyocyte injury and the role of 4,4’-diisothiocyanostilbene-2,2’-disulfonic acid (DIDS), a chloride channel blocker, in the injury. Methods Primarily cultured neonatal rat cardiomyocytes were exposed to glucose (33mmol/L) for 72h to establish the cell model of high glucose-induced injury. The cardiomyocytes were randomly divided into 4 groups: control group, high glucose group, high glucose+DIDS group and DIDS group. MTT assay was applied to detect cell viability, and flow cytometry was used to measure cell viability and apoptosis. N-(Ethoxycarbonylmethyl)-6-methoxyquinolinium bromide (MQAE) was used to examine the intracellular chloride concentration. Results High glucose decreased the cardiomyocyte viability in a dose- and time-dependent manner (P<0.05). Cardiomyocyte injury was mainly in the form of apoptosis. Compared to control group, high glucose resulted in a significant decrease in intracellular Cl- in the cardiomyocytes (P<0.05). There was no significant difference in cardiomyocyte viability and intracellular Cl- between the DIDS treated cells and control cells (P>0.05). While, DIDS treatment improved the cardiomyocyte viability and attenuated the decrease in intracellular Cl- in cardiomyocytes after high glucose induction (P<0.05). Conclusion Cl- is involved in the high glucose-induced cardiomyocyte injury. DIDS attenuates the injury which mainly presents as apoptosis.