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机构地区:[1]中国医科大学附属盛京医院神经内科,辽宁沈阳110004 [2]天津市天和医院脑系科
出 处:《中国老年学杂志》2009年第5期540-542,共3页Chinese Journal of Gerontology
基 金:辽宁省自然科学基金(20052097)
摘 要:目的探讨吡那地尔对大鼠局灶性脑缺血再灌注后Bcl-2和Bax蛋白表达的影响。方法20只Wistar雄性大鼠随机分为假手术组、对照组、KATP开放剂组及KATP开放剂+阻断剂组,每组5只。应用线栓法制备大鼠大脑中动脉缺血模型,应用TUNEL法检测神经元凋亡,应用免疫组化方法检测Bcl-2及Bax蛋白表达,同时观察神经功能缺损评分。结果KATP开放剂组与对照组及KATP开放剂+阻断剂组相比,神经功能缺损程度显著减轻(P<0.05),神经元凋亡数显著减少(P<0.01),Bcl-2蛋白表达显著增多,Bax蛋白表达显著减少(P<0.01),对照组与与KATP开放剂+阻断剂组之间无显著性差异。结论KATP通道开放剂能显著增加脑缺血再灌注后Bcl-2蛋白表达,减少Bax蛋白表达,抑制神经元凋亡,改善神经功能缺损程度,对脑缺血再灌注损伤发挥保护作用。Objective To study the effects of pinacidil on the expressions of Bcl-2 and Bax proteins following focal cerebral ischemia-reperfusion (I/R). Methods 20 male Wistar rats were randomly divided into sham, control, KATP opener, KATP opener + blocker groups. The middle cerebral artery occlusion models were established by intraluminal suture occlusion method, neuronal apoptosis was detected by TUNEL staining, the expressions of Bcl-2 and Bax proteins were tested by immunohistochemical staining, the scores of neurological function deficits were evaluated. Results Compared with control group and KATP opener + blocker group, the scores of neurological function deficits in KATP opener group were significantly less ( P 〈 0. 05 ), the number of apoptotic neurons was significantly decreased ( P 〈 0. 01 ) , the expression of Bcl-2 protein was significantly higher and the expression of Bax protein was significantly lower (P 〈 0.01 ). There were no differences between control group and KATP opener + blocker group ( P 〉 0. 05 ). Conclusions KATP opener has a protective effect on cerebral I/R injury by significantly increasing the expression of Bel-2 protein, decreasing the expression of Bax protein, inhibiting neuronal apoptosis and improving neurological function deficits.
关 键 词:脑缺血 ATP敏感性钾通道 凋亡 BCL-2 BAX 神经功能缺损
分 类 号:R322.81[医药卫生—人体解剖和组织胚胎学]
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