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Role of ATP-sensitive potassium channels in inhibitory effect of hydrogen sulfide on high glucose-induced injury in H9c2 cardiac cells / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 785-790, 2015.
Article in Chinese | WPRIM | ID: wpr-464203
ABSTRACT

AIM:

To investigate the roles of ATP-sensitive potassium ( KATP ) channels in high glucose-induced cardiac injury and the inhibitory effect of hydrogen sulfide ( H2 S) on the cardiomyocyte injury.

METHODS:

The expres-sion level of KATP channel protein was tested by Western blot.The cell viability was measured by CCK-8 assay.The number of apoptotic cells was observed by Hoechst 33258 nuclear staining.Mitochondrial membrane potential ( MMP) was exam-ined by JC-1 staining.

RESULTS:

After the H9c2 cells were treated with 35 mmol/L glucose ( high glucose, HG) for 1~24 h, the protein level of KATP channel was significantly reduced at 6 h, 9 h, 12 h and 24 h, reaching the minimum level at 12 h and 24 h.Pretreatment of the cells with 400μmol/L NaHS ( a donor of H2 S) prior to exposure to HG for 12 h con-siderably blocked the down-regulation of KATP channels induced by HG.Pretreatment of the cells with 100 μmol/L mito-chondrial KATP channel opener diazoxide, 50μmol/L non-selective KATP channel opener pinacidil or NaHS obviously inhibi-ted HG-induced injuries, leading to an increase in the cell viability, and decreases in the number of apoptotic cells and the MMP loss.Pretreatment with 100μmol/L mitochondrial KATP channel antagonist 5-hydroxydecanoic acid or 1 mmol/L non-selective KATP channel antagonist glibenclamide attenuated the above cardioprotective effects of NaHS.

CONCLUSION:

KATP channels mediate the inhibitory effect of H2 S on HG-induced cardiac injury.

Full text: Available Index: WPRIM (Western Pacific) Type of study: Diagnostic study Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2015 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Type of study: Diagnostic study Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2015 Type: Article