Bcl-2和Bax参与内源性一氧化氮对大鼠胃黏膜缺血/再灌注损伤的保护作用

Bcl-2 and Bax participate in the protective role of endogenous nitric oxide in gastric ischemia/reperfusion injury of rat

目的研究Bcl-2和Bax是否参与内源性一氧化氮(nitric oxide,NO)对大鼠胃黏膜缺血/再灌注损伤的保护作用。方法采用大鼠胃缺血/再灌注(gastric ischemia/reperfusion,GI/R)模型(夹闭腹腔动脉30 min后再灌注),应用免疫组织化学、蛋白免疫印迹方法研究NO前体物质左旋-精氨酸(L-arg)和NO合成酶抑制剂L-NG-硝基精氨酸甲酯(L-NAME)对缺血/再灌注后大鼠胃黏膜细胞凋亡、增殖以及Bcl-2、Bax的影响。实验分为4组:GI/R组、L-arg组(L-arg+GI/R)、L-NAME组(L-NAME+GI/R)、L-NAME+L-arg组(L-NAME+L-arg+GI/R),L-NAME和L-arg于手术前20 min一次性腹腔注射。结果与GI/R组相比,L-arg组胃黏膜凋亡细胞减少,增殖细胞增加,Bcl-2阳性细胞百分比和蛋白水平明显升高,Bax显著降低(P<0.05);L-NAME组与GI/R组相比胃黏膜凋亡细胞增加,增殖细胞减少,Bcl-2阳性细胞百分比和蛋白水平明显降低,Bax显著升高(P<0.05);同时给予L-arg和L-NAME对胃的缺血/再灌注损伤无明显影响。结论Bcl-2和Bax参与内源性NO对大鼠胃黏膜缺血/再灌注损伤的保护作用。

Objective To investigate the effects of Bcl - 2 and Bax on the protective role of endogenous nitric oxide （NO） in gastric ischemia/reperfusion （GI/R） injury of rat. Methods The GI/R model was estabhshed by clamping the cehac artery for 30 min and allowing reperfusion for 3 h. The effects of L - arginine （ L - arg, NO synthesis precursor） and L - NAME （NO synthesase blocker） on gastric mucosal cellular apoptosis, proliferation and Bcl - 2 and Bax expression were investigated by using immunohistechemistry and Western blot in SD rats. Results In the L- arg group, the gastric mucosal cellular injury induced by GI/R was significantly alleviated, showing decrease of apoptotic cells, increase of proliferative cells, increase of Bcl 2 expression and decrease of Bax expression, as compared with those in GI/R group （P 〈0.05）. In the L - NAME group, the resultS were the opposite： with the gastric mucosal cellular injury significantly aggravated and accompanied by increase of apoptotic cells, etc （ P 〈 0. 05）. Conclusion Bcl - 2 and Bax participate in the protective role of endogenous nitric oxide in gastric ischemia/reperfusion injury of rat.