论文部分内容阅读
目的 探讨硫化氢(H2S)对大鼠胃缺血/再灌注损伤的保护作用机制.方法 成年大鼠随机分为假手术组、胃缺血/再灌注组以及硫酸氢化钠(NaHS,外源性H2S供体)处理组,采用夹闭大鼠腹腔动脉30 min再灌注1 h的方法 建立大鼠胃缺血/再灌注损伤模型,并测定胃黏膜损伤面积.Western blotting测定胃黏膜细胞中Bcl - 2、Bax以及caspase-3的表达.结果 给予NaHS预处理明显减少胃缺血/再灌注引起的胃黏膜损伤面积(P＜0. 05).与胃缺血/再灌注组相比,NaHS组Bcl-2以及caspase-3的表达显著下降(P＜0. 05).结论 NaHS能明显减轻胃缺血/再灌注损伤,外源性H2S可能通过抑制胃黏膜细胞凋亡通路,发挥保护胃黏膜的作用.“,”Objective To investigate the protective mechanism of hydrogen sulfide (H2S) in rats with gastric ischemia/perfusion injure. Methods Adult rats were randomly divided into a sham group, a gastric ischemia/reperfusion group and an NaHS (H2S exogenous donor) group. Then, a rat model of gastric ischemia/reperfusion injure was established through occlusion of the celiac artery for 30 min followed by 1 h of reperfusion. The area of gastric mucosal damage was measured. The expression of Bcl - 2, Bax and caspase -3 in gastric mucosal cells were determined by Western blotting. Results Pretreatment of NaHS significantly reduced the area of gastric mucosal damage induced by gastric ischemia/reperfusion (P ＜ 0. 05). Meanwhile, NaHS pretreatment inhibited the levels of Bcl - 2, Bax and caspase - 3 compared with the gastric ischemia/reperfusion group (P ＜0. 05). Conclusions NaHS can attenuate gastric ischemia/reperfusion injure. Exogenous H2S may protect gastric mucosa through inhibiting the pathway of apoptosis.