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Hydrogen sulfide protects cardiomyocytes against high glucose-induced injury by modulating leptin espression

Zhang Li-l

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Abstract

Objective To investigate the role of leptin in high glucose(HG)-induced cardiomyocyte injury and whether hydrogen sulfide(H2S) protects cardiomyocytes against HG-induced injury by modulating leptin expression.Methods Cell viability was measured by cell counter kit(CCK-8);The changes in morphology and amount of apoptotic cells were detected by Hoechst nuclear staining;The level of intracellular reactive oxygen species(ROS) was tested by DCFH-DA Staining and photofluorography.Mitochondrial membrane potential(MMP) was observed by rhodamine 123(Rh123) staining followed by photofluorography.The expression of leptin protein was evaluated by Western blot assay.Results Exposure of H9c2 cardiac cells to 35 mmol/L glucose(high glucose,HG) for 9 h markedly enhanced the expression of leptin and induced significant injuries,as evidenced by a decrease in cell viability,the increases in apoptotic cells and ROS generation as well as a loss of MMP.Pretreatment with NaHS(a donor of H2S) inhibited HG-induced upregulation of leptin expression in H9c2 cardiac cells.Pretreatment with either NaHS or leptin antagonist protected H9c2 cardiac cells against the HG-induced injuries mentioned above.Conclusion Leptin is involved in HG-induced cardiomyocyte injury.Exogenous H2S may protect cardioyocytes against HG-induced injuries by modulating leptin expression.

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Objective To investigate the role of leptin in high glucose(HG)-induced cardiomyocyte injury and whether hydrogen sulfide(H2S) protects cardiomyocytes against HG-induced injury by modulating leptin expression.Methods Cell viability was measured by cell counter kit(CCK-8);The changes in morphology and amount of apoptotic cells were detected by Hoechst nuclear staining;The level of intracellular reactive oxygen species(ROS) was tested by DCFH-DA Staining and photofluorography.Mitochondrial membrane potential(MMP) was observed by rhodamine 123(Rh123) staining followed by photofluorography.The expression of leptin protein was evaluated by Western blot assay.Results Exposure of H9c2 cardiac cells to 35 mmol/L glucose(high glucose,HG) for 9 h markedly enhanced the expression of leptin and induced significant injuries,as evidenced by a decrease in cell viability,the increases in apoptotic cells and ROS generation as well as a loss of MMP.Pretreatment with NaHS(a donor of H2S) inhibited HG-induced upregulation of leptin expression in H9c2 cardiac cells.Pretreatment with either NaHS or leptin antagonist protected H9c2 cardiac cells against the HG-induced injuries mentioned above.Conclusion Leptin is involved in HG-induced cardiomyocyte injury.Exogenous H2S may protect cardioyocytes against HG-induced injuries by modulating leptin expression.

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Available abstract

Objective To investigate the role of leptin in high glucose(HG)-induced cardiomyocyte injury and whether hydrogen sulfide(H2S) protects cardiomyocytes against HG-induced injury by modulating leptin expression.Methods Cell viability was measured by cell counter kit(CCK-8);The changes in morphology and amount of apoptotic cells were detected by Hoechst nuclear staining;The level of intracellular reactive oxygen species(ROS) was tested by DCFH-DA Staining and photofluorography.Mitochondrial membrane potential(MMP) was observed by rhodamine 123(Rh123) staining followed by photofluorography.The expression of leptin protein was evaluated by Western blot assay.Results Exposure of H9c2 cardiac cells to 35 mmol/L glucose(high glucose,HG) for 9 h markedly enhanced the expression of leptin and induced significant injuries,as evidenced by a decrease in cell viability,the increases in apoptotic cells and ROS generation as well as a loss of MMP.Pretreatment with NaHS(a donor of H2S) inhibited HG-induced upregulation of leptin expression in H9c2 cardiac cells.Pretreatment with either NaHS or leptin antagonist protected H9c2 cardiac cells against the HG-induced injuries mentioned above.Conclusion Leptin is involved in HG-induced cardiomyocyte injury.Exogenous H2S may protect cardioyocytes against HG-induced injuries by modulating leptin expression.

Key concepts: Leptin, Viability assay, Chemistry, Reactive oxygen species, Western blot, Downregulation and upregulation, Apoptosis, Intracellular

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