丁苯酞对大鼠局灶性脑缺血再灌注损伤后脑程序性凋亡因子-5表达的影响

目的研究丁苯酞对大鼠局灶性脑缺血再灌注损伤后程序性细胞凋亡因子-5表达的影响。方法健康雄性SD大鼠132只，随机分为假手术组、缺血再灌注模型组、缺血再灌注治疗组，后两者再分别分为再灌注6h、24h、48h、3d、7d共5个亚组，每亚组12只。应用大脑中动脉线栓法制作大鼠局灶性脑缺血再灌注模型，治疗组造模成功后即刻给予丁苯酞80mg／（kg·d）灌胃，余各大鼠给予同剂量生理盐水灌胃。在相应时间点评定神经功能缺损评分，TTC染色法测定脑梗死体积，免疫组化法测定缺血脑组织PDCD-5的表达，TUNEL法测定凋亡细胞。结果假手术组未见梗死灶，偶有凋亡细胞，少见PDCD-5的表达；模型组及治疗组均可见梗死灶及凋亡细胞，有PDCD-5的表达；治疗组在对应时间点较模型组梗死灶小，凋亡细胞少，PDCD-5的表达少。结论丁苯酞对局灶性脑缺血再灌注损伤具有保护作用，其机制可能是通过减少PDCD-5的表达抑制细胞凋亡。

Effect of butylphthalide on the expression of programmed cell death factor-5 in rats With focal cerebral ische- mia reperfusion injury

Objective To study the effect of butylphthalide on the expression of PDCD-5 （programmed cell death factor-5） in rats with focal cerebral ischemia reperfusion injury. Methods One hundered and thirty-two healthy male Sprague-Dawley rats were randomly divided into operated group, model group and treatment group. The latter two groups were separately sub-di- vided into reperfusion subgroup at 6th hour, 24th hour, 48th hour, 3rd day and 7th day. There were 12 rats in each subgroup. Rats were selected to establish focal cerebral isehemia reperfusion model by middle cerebral artery thread embolism method. Af- ter successful modeling, the treatment group was applied instantly by gavage with butylphthalide（80 mg · kg 1 . d 1 ）, while the rest groups were given by gavage with equal volume of saline. The neurological deficit scores of rats in each group were respec- tively conducted at different time points. The PDCD-5 expression in brain tissue was detected by immunohistochemistry method and the infarct sizes were measured with TTC staning. Results There was no infarct, few expression of apoptosis or PDCD-5 in operated group. PDCD-5-positive cells and apoptotic cells could be found in both model group and treatment group. In treat- ment group, the infarct was smaller and PDCD-5-positive cells and apoptotic cells was fewer than model group（P〈0.05）. Con- clusion Butylphthalide plays a protective role on focal cerebral ischemia reperfusion injury and the mechanism might be related to the reduction of PDCD-5 expression.