Protective effects of Cx43-mediated exogenous hydrogen sulfide postconditinoing on rat hearts
Ping Wang
Abstract
Ping Wang
Abstract
Aim To investigate whether connexin 43(Cx43) mediated hydrogen sulfide postconditioning protects isolated rat hearts against ischemia/reperfusion(I/R)injury.Methods 72 male SD rat hearts were isolated and linked to the Langendorff apparatus.They were randomly divided into 6 groups(n=12):sham group(Sham),ischemia /reperfusion group(I /R),DMSO group(DMSO),18β-AGA group(AGA),hydrogen sulfide postconditioning group(NP),and hydrogen sulfide with 18β-AGA group(N + A).The heart rate(HR),the left ventricular diastolic pressure(LVEDP),the left ventricular developed pressure(LVDP),the maximum rate of increase or decrease of left ventricular pressure(±dp/dtmax) were recorded at 20 min of equilibrium and 60 min of reperfusion respectively.Myocardial infarct size was measured by triphenyl tetrazolium chloride(TTC) staining.The expression of total Cx43(tCx43) and phosphorylated Cx43(pCx43) in mitochondria and cytosol were determined with Western blot analysis at the end of reperfusion.Results There were no differences in baseline hemodyamics observed among the experimental groups(P0.05).After reperfusion,compared with I/R group,NP group had better hemodynamics,the myocardial infarct size was much lower(P0.05),the expression of tCx43 in mitochondria increased significantly,but decreased significantly in cytosol,the expression of pCx43 was same to tCx43.However,18β-AGA abolished the cardioprotective effects offered by hydrogen sulfide postconditioning and decreased tCx43 and pCx43 expression in mitochondria(P0.05).Conclusion Exogenous hydrogen sulfide postconditioning effectively protects isolated rat hearts against ischemia and reperfusion injury via activating Cx43.
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Aim To investigate whether connexin 43(Cx43) mediated hydrogen sulfide postconditioning protects isolated rat hearts against ischemia/reperfusion(I/R)injury.Methods 72 male SD rat hearts were isolated and linked to the Langendorff apparatus.They were randomly divided into 6 groups(n=12):sham group(Sham),ischemia /reperfusion group(I /R),DMSO group(DMSO),18β-AGA group(AGA),hydrogen sulfide postconditioning group(NP),and hydrogen sulfide with 18β-AGA group(N + A).The heart rate(HR),the left ventricular diastolic pressure(LVEDP),the left ventricular developed pressure(LVDP),the maximum rate of increase or decrease of left ventricular pressure(±dp/dtmax) were recorded at 20 min of equilibrium and 60 min of reperfusion respectively.Myocardial infarct size was measured by triphenyl tetrazolium chloride(TTC) staining.The expression of total Cx43(tCx43) and phosphorylated Cx43(pCx43) in mitochondria and cytosol were determined with Western blot analysis at the end of reperfusion.Results There were no differences in baseline hemodyamics observed among the experimental groups(P0.05).After reperfusion,compared with I/R group,NP group had better hemodynamics,the myocardial infarct size was much lower(P0.05),the expression of tCx43 in mitochondria increased significantly,but decreased significantly in cytosol,the expression of pCx43 was same to tCx43.However,18β-AGA abolished the cardioprotective effects offered by hydrogen sulfide postconditioning and decreased tCx43 and pCx43 expression in mitochondria(P0.05).Conclusion Exogenous hydrogen sulfide postconditioning effectively protects isolated rat hearts against ischemia and reperfusion injury via activating Cx43.
Key concepts: Hydrogen sulfide, Preload, Ventricular pressure, Western blot, Reperfusion injury, Chemistry, Internal medicine, Tetrazolium chloride