中文摘要：

目的 研究瞬时受体电位香草酸亚型1（TRPV1）对离体小鼠心脏缺血/再灌注（I/R）后心肌细胞凋亡的影响及与PI3K/Akt通路的关系。方法 TRPV1基因敲除（TRPV1^-/-）和野生型（WT）小鼠各54只,均各随机分为假手术组（sham）、缺血再灌注组（I/R）和LY294002处理组（LY）。建立Langendorff离体心脏灌注模型,检测心功能;灌注结束后,TTC染色法检测心肌梗死面积;TUNEL法检测心肌细胞凋亡;Western blot检测Bcl-2、Bax、Akt和p-Akt的蛋白表达水平。结果 I/R后,TRPV1^-/-小鼠较WT小鼠的LVDP明显降低（P〈0.001）,LVEDP明显升高（P〈0.001）,同时心肌梗死面积和心肌凋亡细胞明显增加（P〈0.01）,Bcl-2/Bax和p-Akt表达水平下降（P〈0.001）。LY294002阻断PI3K后,与相应的I/R组相比,WT小鼠心肌梗死面积明显扩大（P〈0.001）,心肌凋亡细胞明显增加（P〈0.01）,Bcl-2/Bax和p-Akt蛋白表达水平降低（P〈0.001）。结论 TRPV1可能通过PI3K/Akt通路抑制离体小鼠心脏缺血/再灌注所致的心肌细胞凋亡。

英文摘要：

Objective To investigate the effects of TRPV1 on myocardial apoptosis and PI3K/Akt expression during ischemia/reperfusion injury in mice. Methods Totally 54 wild type （WT） mice and 54 TRPVl-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 apopto- sis was detected by TUNEL. Expression of Bcl-2, Bax, Akt and p-Akt was measured by Western blot. Infarct size was measured by TFC 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）, PV1^-/- ＋ I/R the PI3K with minished exp I/R-induced Key words ： while the proportion of apoptotic cardiomyocytes and infarct size significantly increased in the TR- group as compared with the WT ＋ I/R group （P 〈 0. 01 ）. Compared with I/R group, blockade of LY294002 significantly increased the apoptosis index （P 〈 0. 01 ）, infarct size （P 〈0. 001 ） and di- ssion of Bcl-2/Bax and p-Akt in WT ＋ LY group （P 〈 0. 001 ）. Conclusions TRPV1 may attenuate apoptosis in isolated heart through PI3K/Akt signaling pathway .