| Objective: To study the effect of hydrogen sulfide on gene and protein expression of myosin light chain kinase(MLCK) and membrane KATP channel in cardiomyocytes of diabetic rats, so as to illustrate the molecular mechanism of hydrogen sulfide protective effect on myocardial injury in diabetic rats.Methods: Forty male SD rats were randomly divided into normal control group(NC group), diabetic control group(DM group), Na HS treatment group(Na HS+DM group)and Na HS control group(Na HS group). Diabetic models were established by streptozotocin(STZ) 55mg/kg intraperitoneal, monitoring of blood glucose continues above 16.7 mmol/L for diabetic rats. From the 7th week, NC group and DM control group were treated with 0.5% Na HS 10 ml/kg/d, Na HS+DM group and Na HS group were given Na HS 120 mg/kg/d for 6 weeks. After seven weeks, the heart was perfused in vitro, the body weight of rats being weighted and the coefficient of the heart being calculated. Taking the ventricular muscle tissue, the gene express of MLCK and the KATP channel composed of subunit sulfonylurea receptor(SUR2) and inward rectifier potassium channel(Kir6.2) in the cardiomyocytes were detected by RT-PCR. The protein express of MLCK, ROCK, Rho in the cardiomyocytes were detected by Western blotting.Results:(1) The weight of DM group and NaHS+DM group was significantly lower than normal group. The weight of NC group and Na HS group rats increased significantly. Compared with DM group, the weight of Na HS+DM group improved significantly(P < 0.05).(2) Compared with the NC group, the maximum increase /decrease rate of left ventricular pressure(±dp/dtmax), left ventricular development pressure(LVDP) rate, and left ventricular end diastolic pressure(LVEDP) of DM group decreased significantly(P < 0.01). Those of Na HS+DM group increased significantly compared with the NC group(P < 0.01, P < 0.05).(3) Compared withNC group, the expressions of MLCK, SUR2, Kir6.2 m RNA in DM group were decreased(P < 0.01). Compared with DM group, the expressions of MLCK, SUR2,Kir6.2 m RNA in Na HS+DM group increased(P < 0.01), and there was no significant difference in NC group and Na HS group(P > 0.05).Conclusion: H2 S can improve the general condition of the myocardium of diabetic rats, improve left ventricular function and the gene expression of MLCK of diabetic rats. Its mechanism may be that H2 S regulates the MLCK cytoskeleton contraction.The expression of ROCK, Rho and MLCK protein in diabetic cardiomyopathy rats increased treated with hydrogen sulfide. It may regulate Rho/ROCK/MLCK signaling pathway so as to increase the phosphorylation level of MLCK to regulate the systolic and diastolic function of cardiocyte in diabetic cardiomyopathy. The gene expression of KATP channels of myocardial membrane increased treated with hydrogen sulfide. In order to elucidate the molecular mechanism of protective effects of hydrogen sulfide on diabetic cardiomyopathy. |
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