Abstract:【Abstract】Objective To investigate the effect and mechanism of DEX on oxidative stress and apoptosis induced by high glucose in cardiomyocytes. Methods The cardiomyocyte H9C2 was cultured in vitro, and a high glucose injury model was established. The cardiomyocytes were treated with DEX with different concentrations (5 μg/L, 10 μg/L, 20 μg/L),respectively,which were recorded as experiment 1 group, experiment 2 group, experiment 3 group. The contents of LDH, MDA and SOD were detected. qRTPCR was used to detect the expression of miR126. miRNC, miR126 mimcis, antimiRNC, and antimiR126 were transfected into cardiomyocytes, respectively, with DMEM medium containing 35 mmol/L glucose and 20 μg/L DEX to cultivate. Flow cytometry was used to detect the apoptosis rate. Western blot was used to detect the expression of procaspase3 and clcaspase3. Results Compared with the control group, the levels of LDH and MDA in the high glucose injury model group were significantly increased (P<0.05), the content of SOD was significantly reduced (P<005), the expression level of miR126 was significantly reduced (P<005), and the apoptosis rate was significantly increased (P<005), the level of clcaspase3 protein was significantly increased (P<005), and the level of procaspase3 protein was significantly decreased (P<005). Compared with the high glucose injury model group, the contents of LDH and MDA in experimental group 1, experimental group 2 and experimental group 3 were significantly reduced (P<005), the content of SOD was significantly increased (P<005), and the expression level of miR126 was increased (P<005), the apoptosis rate was significantly reduced (P<005), the level of clcaspase3 protein was significantly reduced (P<005), and the level of procaspase3 protein was significantly increased (P<005). There was a statistically significant difference in each index among the experimental group 1, the experimental group 2, and the experimental group 3 (P<005). Compared with miRNC group, the content of LDH and MDA in miR126 group was significantly reduced (P<005), the content of SOD was significantly increased (P<005), and the apoptosis rate was significantly reduced (P<005), the level of caspase3 protein was significantly reduced (P<005), and the level of procaspase3 protein was significantly increased (P<005). Overexpression of miR126 could enhance the effect of DEX on high glucoseinduced oxidative stress and apoptosis in myocardial cells, and inhibition of miR126 expression could attenuate the effect of DEX on high glucoseinduced oxidative stress and apoptosis in cardiac muscle cells. Conclusion DEX could inhibit the oxidative stress and apoptosis of cardiomyocytes induced by high glucose by upregulating the expression of miR126.