摘要目的 探讨丁苯酞对脑缺血再灌注损伤的保护作用和可能机制.方法 60只健康清洁级成年Sprague-Dawley大鼠,随机分为假手术组、生理盐水对照组、小剂量丁苯酞组和大剂量丁苯酞组,每组15只.应用线栓法建立局灶性脑缺血再灌注模型.再灌注开始时,小剂量丁苯酞组和大剂量丁苯酞组分别腹腔注射丁苯酞注射液100 mg/k和400 mg/kg,假手术组和生理盐水组分别腹腔注射生理盐水0.5 ml/kg.所有大鼠在缺血再灌注24h后处死.结果 小剂量丁苯酞组(t=1.488,P=0.000)和大剂量丁苯酞组(=2.362,P=0.000)神经功能缺损程度较生理盐水组均显著性改善,其中大剂量丁苯酞组较小剂量丁苯酞组改善更为显著(t=-0.873,P=0.000).小剂量丁苯酞组(t=18.589,P=0.000)和大剂量丁苯酞组(=36.963,P=0.000)脑梗死体积较生理盐水对照组显著性缩小,其中大剂量丁苯酞组梗死体积较小剂量丁苯酞组缩小更显著(t=-18.374,P=0.000).HE染色显示,生理盐水对照组神经元稀疏、大量变性坏死,细胞间隙增大,细胞间质空泡样改变.丁苯酞组神经元变性坏死明显减少,存活神经细胞增多,大剂量丁苯酞组改善更为显著.小剂量丁苯酞组和大剂量丁苯酞组SOD活性较假手术组和生理盐水对照组显著性增高(P均＜0.05),其中大剂量丁苯酞组SOD活性显著性高于小剂量丁苯酞组(t=80.199,P=0.000)；小剂量丁苯酞组和大剂量丁苯酞组MDA水平较假手术组和生理盐水对照组显著性降低(P均＜0.05),其中大剂量丁苯酞组MDA水平显著性低于小剂量丁苯酞组(t=-1.308,P=0.000).结论 丁苯酞对缺血再灌注损伤的保护作用可能与机体抗氧化活性增强有关.

abstractsObjective To investigate the protective effect of butylphthalide for focal cerebral ischemiareperfusion injury and its possible mechanism.Methods A total of 60 healthy and clean adult Sprague-Dawley rats were randomly divided into sham operation,saline control,low-dose butylphthalide and high-dose butylphthalide groups (n =15 in each group).A focal cerebral ischemia-reperfusion model was induced by the suture method.At the beginning of reperfusion,100 rng/kg and 400 mg/kg butylphthalide injection were injected intraperitoneally in the rats of the low-dose butylphthalide and high-dose butylphthalide groups; 0.5 ml/kg saline was injected intraperitoneally in rats of the sham operation and saline control groups.All the rats were sacrificed after 24 h of ischemia-reperfusion.Results The degree of neurological deficit in the low-dose butylphthalide (t =1.488,P =0.000) and high-dose butylphthalide (t =2.362,P =0.000) groups were significantly improved compared to the saline control group,in which the high-dose butylphthalide group was improved more significantly than the low-dose butylphthalide group (t =-0.873,P =0.000).The infarct volume in the low-dose butylphthalide (t =18.589,P =0.000) and high-dose butylphthalide (t =36.963,P =0.000) groups were reduced significantly compared to the saline control group,in which the infarct volume of the high-dose butylphthalide group was reduce more significantly than that of the low-dose butylphthalide group (t =-18.374,P =0.000).HE staining showed that neurons were sparse,there were a large number of degeneration and necrosis,cell space became larger,and the intercellular substances showed vacuolar changes.In the butylphthalide group,the neuronal degeneration and necrosis reduced significantly,the survival of nerve cells increased,and the improvement of the high-dose butylphthalide group was more remarkable.SOD activity of the low-dose and high-dose butylphthalide groups were increased significantly compared to the sham operation and saline control groups (all P ＜0.05),in which the SOD activity in the high-dose butylphthalide group was significantly higher than that in the low-mall dose butylphthalide group (t =80.199,P =0.000); The MDA levels in the low-dose and high-dose butylphthalide groups were decreased significantly compared to the sham operation and saline control groups (all P ＜ 0.05),in which the MDA level in the high-dose butylphthalide group was significantly lower than that in the low-dose butylphthalide group (t =-1.308,P=0.000).Conclusions The protective effect of butylphthalide on ischemia-reperfusion injury may be associated with the increased antioxidant activity.