关键词: 关键词：心肌缺血/再灌注损伤, 瞬时受体电位香草酸通道, PI3K/Akt, 凋亡

Abstract: 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 Compared with the WT + I/R group, the LVEDP significantly increased, and LVDP significantly decreased in the TRPV1-/- + I/R group (P < 0.001). 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 significantly in the TRPV1-/- + I/R group as compared with the WT + I/R group (P < 0.01). Compared with I/R group, blockade of the PI3K 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.

Key words: Key words: myocardial ischemia/reperfusion injury, transient receptor potential vanilloid channel, PI3K/Akt, apoptosis