Effect of TRPV1 on the apoptosis of H9c2 cardiomyocyte after hypoxia-reoxygenation injury and its mechanism

Objective To investigate the protective effect and possible mechanism of transient receptor potential cation channel subfamily V member 1 (TRPV1) on apoptosis of H9c2 cardiomyocyte after hypoxia-reoxygenation injury. Methods H9c2 cardiomyocyte were randomly divided into control group, model group (hypoxia/reoxygenation), capsaicin group (hypoxia/reoxygenation + capsaicin), capsaicin + LY group (hypoxia/reoxygenation + capsaicin + LY294002). The cell survival rate of cardiomyocyte was determined by CCK-8 method. The apoptosis rate of cardiomyocyte was determined by flow cytometry. Western blot and reverse transcription-polymerase chain reaction (RT-PCR) were used to determine caspase-3, B-cell lymphoma 2 gene (Bcl-2), Bcl-2 related X protein (BAX), phosphoric acid- protein kinase B (p-Akt) and protein kinase B (Akt) levels. Results Compared with the control group, the cell survival rate of cardiomyocyte and the Bcl-2 level in the model group, capsaicin group and capsaicin + LY group decreased (all P<0.05), the apoptosis rate and the levels of caspase-3, Bax, p-Akt increased (all P<0.05); Compared with the model group, the cell survival rate of cardiomyocyte and the levels of Bcl-2, p-Akt in the capsaicin group were increased (all P<0.05), and the apoptosis rate and the levels of caspase-3 and Bax were decreased (all P<0.05). There were no significant difference in each indexes between the model group and the capsaicin + LY group (all P>0.05). Conclusion TRPV1 can inhibit H9c2 cardiomyocyte apoptosis after hypoxia-reoxygenation inury, and its mechanism may be related to TRPV1 activation of phosphatidylinositol 3-kinase (PI3k)/Akt signaling pathway.