Abstract: Abstract: Objective To investigate the protective effects and the related mechanism of exogenous H2S on diabetic cardiomyopathy (DCM) in rats. Methods Intraperitoneal injection of streptozotocin and diabetic diet were used in healthy male Sprague-Dawley rats were used to establish DCM models. Sixteen DCM rats and 16 normal rats were randomly divided into the following four groups with 8 rats per group: DCM+ saline group, DCM+NaHS group, Control + saline group and Control+NaHS group. DCM+NaHS group rats and Control+NaHS group rats were intraperitoneally administered H2S donor sodium hydrosulfide (NaHS) at a dose of 100 μmol/kg per day for 12 weeks. DCM+saline group rats and Control+saline group rats were intraperitoneally injected with an equivalent volume of physiological saline for 12 weeks. At the end of the experiment, all rats were tested with ultrasonic cardiogram to evaluate the heart function. Then, the left heart ventrucular tissues were collected after executing all rats to be embedded in paraffin and be preserved at - 80 ℃ . The cardiac pathological changes were observed by hematoxylin and eosin staining. The protein expressions of Bcl-2, p-FoxO1, p-JNK were detected by Western blot assay. Results The type of rat model and interving measure showed an effect on the cardiac function, as well as Bcl-2, p-FoxO1 and p-JNK; There was an interaction between the type of rat model and interving measure during the experiment. In DCM group, the levels of LVEF and LVFS values and expressions of Bcl-2 and p-FoxO1 were declined, but the expression of p-JNK was increased. The heart function and cardiac pathological changes were improved in NaHS group. Likewise, expressions of Bcl-2 and p-FoxO1 were upregulated, the expression of p-JNK was downregulated. Conclusion DCM myocardial injury is associated with cell apoptosis. NaHS can alleviate DCM myocardial injury and protect cardiac function, possibly by acting on JNK/FoxO1/Bcl-2 pathway.

Key words: cardiomyopathies, diabetes complications, hydrogen sulfide, apoptosis, Bcl-2, FoxO1, JNK