Abstract: Objective To determine whether heme oxygenase-1 (HO-1) plays a major role in modulating diabetic cardiomyopathy (DCM) and the mechanisms involved in this process. Methods: HO-1 transgenic mice (HO-1 / DM) and wild type mice (Wt / DM) diabetes model were established by conventional intraperitoneal injection of streptozotocin. After eight weeks, echocardiography was used to detect left ventricular function in mice. Left ventricular myocardium was detected by HE staining and the expression of IL-6, TNF-α, Gpx3 and p47 phox mRNA were detected by RT-qPCR. H9C2 cells were cultured in high glucose and were overexpressed HO-1 to observe its effect on ROS production. Results: Compared with Wt/Con mice, the blood glucose, food intake, water intake and urine output were significantly increased and the body weight was significantly decreased in Wt/DM and HO-1/DM mice. Compared with Wt/Con mice left ventricular function was significantly impaired in Wt/DM mice. Left ventricular function was better in HO-1/DM mice than in Wt/DM mice. Wt/DM mice myocardial structure disorder and inflammatory reaction cell infiltration. Compared with Wt/DM mice myocardial structure tends to be normal in HO-1/DM mice. In the Wt/DM mice, the expression of IL-6, TNF-α, Gpx3 and p47phox were higher than the Wt/Con mice (p<0.05), overexpression of HO-1 significantly inhibited this phenomenon. Conclusion: This study demonstrates that HO-1 is cardioprotective in the context of diabetic cardiomyopathy.

Key words: diabetes cardiomyocyte, heme oxygenase-1, oxidative stress, inflammation