TRPV1 Inhibits Apoptosis Mediated By PI3K/Akt Signaling Pathway In Myocardial Ischemia/Reperfusion Mouse Heart

Objective To investigate the effects of TRPV1 on myocardial apoptosis and PI3K/Akt expressions during ischemia/reperfusion injury in mice.Methods 54 wild type（WT） mice and 54 TRPV1-null mutant(TRPV1^-/-) mice were randomly divided into six groups: WT + Sham group, TRPV1^-/- + Sham group, WT + I/R group, TRPV1^-/- + I/R group, WT + LY group and TRPV1^-/- + LY group. The mice hearts were perfused with a Langendorff apparatus and the indexes of cardiac mechanical function were measured. Cardiomyocyte apoptosis was detected by TUNEL. Expression of Bcl-2, Bax, Akt and P-Akt was measured by Western blot. Infarct size was measured by TTC staining.Results The expression of Bcl-2/Bax and P-Akt in the myocardium of the TRPV1^-/- + I/R group was significantly lower than that of the WT + I/R group（P < 0.001）, while the proportion of apoptotic cardiomyocytes and infarct size increased meaningfully in the TRPV1^-/- + I/R group as compared with the WT + I/R group（P < 0.01）. Compared with the I/R group, blockade of the PI3 K with LY294002 significantly increased the apoptosis index（P < 0.01）, infarct size（P < 0.001） and diminished expression of Bcl-2/Bax and P-Akt in WT + LY group（P < 0.001）.Conclusion TRPV1 could attenuate I/R-induced apoptosis in the isolated heart probably through PI3K/Akt signaling pathway.