亚硒酸钠对脑缺血再灌注损伤大鼠HIF-1α表达的影响

目的 研究亚硒酸钠对大鼠脑缺血再灌注损伤后海马神经细胞凋亡的保护作用及其对低氧诱导因子-1α(HIF-1α)表达的影响.方法 48只SD大鼠随机分为假手术组、缺血再灌注组(模型组)及亚硒酸钠治疗组,每组16只,采用线栓法建立脑缺血再灌注模型,治疗组于再灌注后给予亚硒酸钠0.625 mg/(kg·d)腹腔注射7 d.各组大鼠经组织处理后用亚甲兰尼氏体染色及TUNEL染色,分别观察大鼠海马CA1区神经元存活和凋亡情况,Western Blot实验测定缺血组织HIF-1α水平的表达.结果 脑缺血再灌注损伤大鼠海马神经元数目明显减少,凋亡细胞明显增加(P<0.001),亚硒酸钠治疗后海马神经细胞存活数目明显增多,凋亡细胞明显减少(P<0.01);与假手术组比较,模型组大鼠海马HIF-1α水平表达明显增加(P<0.01),而经亚硒酸钠治疗后大鼠海马HIF-1α水平表达较模型组明显降低(P＜0.05).结论 亚硒酸钠可减轻脑缺血再灌注损伤大鼠神经元凋亡,同时能抑制组织HIF-1α的过度表达.

Effects of sodium selenium on the expression of hypoxia inducible factor-1α in rats with cerebral ischemia-reperfusion injury

Objective To investigate the protective effect of sodium selenium on neuronal apoptosis in hippocampus and expression of hypoxia inducible factor-1α(HIF-1α) in rats with cerebral ischemia-reperfusion injury.Methods Totally 48 SD rats were randomly divided into three groups: sham-surgery group,ischemia reperfusion group(model group),and sodium selenite treatment group,each group of 16 rats.In the latter two groups,cerebral ischemia-reperfusion injury was induced by middle cerebral artery occlusion.The rats in treatment group were treated with sodium selenite injection intraperitoneally once a day.Seven days later,the number of neuronal survival was observed by Nissl body methylthionine staining and the number of apoptosis neurons was detected by TUNEL stain in the CA1 hippocampus.The level of HIF-1α protein expression was measured by Western Blot test.Results The number of hippocampal neuron was sharply reduced and the number of apoptotic cell was significantly increased after cerebral ischemia-reperfusion injury in rats(P<0.001),but the survival neurons increased and apoptotic cells decreased significantly in the treatment group(P<0.01).Compared with sham surgery group,the level of HIF-1α protein expression in the hippocampal tissues increased significantly in model group,but it decreased significantly in selenium-treated group compared with model group(P<0.05).Conclusion Sodium selenite can reduce neuronal apoptosis after cerebral ischemia and reperfusion injury in rats,and inhibit that HIF-1α expresses excessively.