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目的研究亚硒酸钠对肾缺血再灌注损伤诱导细胞凋亡的影响。方法18只SD大鼠随机分成3组,假手术组、缺血再灌注组和亚硒酸钠组。采用双侧夹闭大鼠肾蒂的方法制备动物模型,亚硒酸钠组大鼠术前连续3d腹腔注射亚硒酸钠(0.5mg·kg-1)。观察大鼠肾功能、肾脏病理改变,TUNEL及流式细胞术检测肾脏细胞凋亡情况,Western blot分析c-Jun N端蛋白激酶(JNK)、p38丝裂原活化蛋白激酶(p38)、原癌基因c-Jun(c-Jun)的激活和表达。结果缺血再灌注组大鼠血清肌酐(Scr)和尿素氮(BUN)水平,细胞凋亡率及凋亡细胞数量,以及JNK、p38、c-Jun活性明显高于假手术组(P<0.01)。亚硒酸钠组大鼠血清Scr和BUN,细胞凋亡率,凋亡细胞数量,以及JNK、p38、c-Jun活性低于缺血再灌注组,差异有显著意义(P<0.05,P<0.01)。结论亚硒酸钠可能通过下调JNK、p38通路的激活,拮抗肾缺血再灌注损伤诱导的细胞凋亡,从而改善缺血再灌注损伤。
Objective To study the effects of sodium selenite on renal cell apoptosis induced by renal ischemia-reperfusion injury. Methods Eighteen SD rats were randomly divided into three groups: sham operation group, ischemia reperfusion group and sodium selenite group. Animal models were established by bilateral clamping of rat’s renal pedicle. Rats in sodium selenite group were injected intraperitoneally with sodium selenite (0.5 mg · kg -1) for 3 consecutive days. The renal function, renal pathological changes were observed, TUNEL and flow cytometry were used to detect the apoptosis of renal cells. Western blot analysis was used to detect the expression of c-Jun N-terminal protein kinase (JNK), p38 mitogen-activated protein kinase (p38) Activation and expression of gene c-Jun (c-Jun). Results The levels of serum creatinine (Scr) and blood urea nitrogen (BUN), apoptosis and the number of apoptotic cells, as well as JNK, p38 and c-Jun in ischemia-reperfusion group were significantly higher than those in sham operation group ). The activity of Scr and BUN, the apoptosis rate, the number of apoptotic cells, JNK, p38 and c-Jun in selenite group were lower than those in ischemia-reperfusion group (P <0.05, P < 0.01). Conclusion Sodium selenite may reduce ischemia-reperfusion injury by down-regulating the activation of JNK and p38 pathway and antagonizing the apoptosis induced by renal ischemia-reperfusion injury.