【摘 要】
：
目的：国内外大量研究证实,炎症反应在脑缺血再灌注后的病理发展进程及继发性脑损伤中扮演关健角色.氟比洛芬能够减轻啮齿类动物的局灶性或全脑缺血性损伤,但其确切的药物作用机制并不清楚.本研究重点观察NFκB信号通路在氟比洛芬抑制大鼠局灶性脑缺血再灌注炎症反应中的作用.方法：健康雄性Wistar大鼠60只,体重260～310 g,采用随机数字表法,将其随机分为5组(n=12)：假手术组(S组)、脂微球溶剂
【出 处】
：
中国中西医结合麻醉学会年会暨第二届全国中西医结合麻醉学术研讨会
论文部分内容阅读
目的：国内外大量研究证实,炎症反应在脑缺血再灌注后的病理发展进程及继发性脑损伤中扮演关健角色.氟比洛芬能够减轻啮齿类动物的局灶性或全脑缺血性损伤,但其确切的药物作用机制并不清楚.本研究重点观察NFκB信号通路在氟比洛芬抑制大鼠局灶性脑缺血再灌注炎症反应中的作用.方法：健康雄性Wistar大鼠60只,体重260～310 g,采用随机数字表法,将其随机分为5组(n=12)：假手术组(S组)、脂微球溶剂组(V组)、缺血再灌注组(I/R组)、氟比洛芬酯5mg/kg组(F-L组)和氟比洛芬酯10mg/kg组(F-H组).改良线栓法制作大鼠大脑中动脉闭塞(MCAO)2h/再灌注24h动物模型.再灌注即刻F组经尾静脉分别注射氟比洛芬酯5mg/kg和10 mg/kg,V组尾静脉注射脂微球溶剂1 ml/kg,S组和I/R组尾静脉注射给药等容量生理盐水.于再灌注24 h时常规HE染色观察各组缺血脑皮层病理变化情况；Rt-PCR法测定各组缺血脑皮层区炎性细胞因子IL-1β、IL-6、TNF-α的mRNA变化；分光光度法测定各组髓过氧化物酶活性；采用Western blot和免疫组化方法检测各组缺血脑皮层p-NF-κB(p65)表达变化.结果：与S组比较,IR组、V组和F组神经功能缺陷评分和细胞凋亡指数升高,IR组和V组脑皮层区Bc1-2蛋白表达下调,Bax蛋白表达上调,Bc1-2/Bax比降低(P＜0.05)；与IR组比较,V组各指标差异无统计学意义(P＞0.05),F组神经功能缺陷评分和细胞凋亡指数降低,脑皮层区Bc1-2蛋白表达上调,Bax蛋白表达下调,Bc1-2/Bax比升高(P＜0.05).结论：氟比洛芬酯后处理可上调局灶性脑缺血再灌注损伤大鼠缺血侧脑皮层区Bc1-2蛋白的表达,下调Bax蛋白的表达,纠正Bc1-2与Bax的失衡,抑制细胞凋亡,从而减轻大鼠局灶性脑缺缺血脑皮层血再灌注损伤.
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