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目的探讨潘妥洛克减轻胃缺血-再灌注(I/R)损伤和凋亡途径的关系。方法C57BL/6小鼠随机分为假手术组、模型组(溶剂+手术组)、给药组(潘妥洛克+手术组),每组10只。夹闭小鼠腹腔动脉30min后松开动脉夹再灌注1h制作胃I/R模型,根据分组情况于手术前1h腹腔注射溶剂10ml/kg或2mg/ml的潘妥洛克溶液10ml/kg。再灌注1h后取胃标本铺平,拍照软件分析计算出血百分比。应用蛋白免疫印迹法检测比较各组Caspase-8、分裂型Caspase-3、Bax、Bcl-2、丝氨酸/苏氨酸蛋白激酶(AKT)以及磷酸化AKT的表达水平。结果给药组胃黏膜糜烂出血面积明显减少,与模型组比较差异有统计学意义(P<0.01);给药组凋亡相关蛋白Caspase-8、分裂型Caspase-3、Bax及Bcl-2与模型组相比无明显差异,而上游促修复抑制凋亡的关键信号蛋白AKT的磷酸化水平比模型组明显降低(P<0.01)。结论潘妥洛克减轻胃缺血-再灌注损伤不依赖于抑制Caspase-3促凋亡途径,而可能与潘妥洛克抑制AKT的磷酸化有关。
Objective To investigate the relationship between the changes of peritoneal on gastric ischemia-reperfusion (I / R) injury and apoptotic pathways. Methods C57BL / 6 mice were randomly divided into sham-operated group, model group (solvent + surgery group) and drug-treated group (treated group). After occlusion of the celiac artery in mice for 30min, the artery clamps were released and reperfusion for 1h to make the gastric I / R model. According to the grouping conditions, intraperitoneal injection of 10ml / kg or 10mg / ml of pentropole solution 10ml / kg 1h prior to surgery. 1h after reperfusion, gastric specimens were taken to pave the way, taking pictures of software analysis to calculate the percentage of bleeding. Western blotting was used to detect the expression of Caspase-8, Caspase-3, Bax, Bcl-2, Serine / Threonine protein kinase (AKT) and phosphorylated AKT in each group. Results The bleeding area of gastric mucosal erosion in treatment group was significantly decreased compared with model group (P <0.01). Caspase-8, Caspase-3, Bax and Bcl-2 There was no significant difference between model group and model group, but the phosphorylation level of AKT, a key signal protein that promotes apoptosis in the upstream, was significantly lower than that in model group (P <0.01). CONCLUSION: The alteration of gastric ischemia-reperfusion injury induced by peritone in rats is not dependent on the pro-apoptotic pathway of Caspase-3, but may be related to the inhibition of the phosphorylation of PTT by PTT.