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目的:观察参芎化瘀胶囊预处理对大鼠脑缺血再灌注损伤后血管内皮生长因子(vascular endothelial growthfactor,VEGF)表达的影响,探讨参芎化瘀胶囊对大鼠急性脑缺血再灌注损伤保护作用的机制。方法:实验大鼠随机分为:假手术组、缺血再灌注组、参芎化瘀胶囊高、中、低剂量预处理组(480,240,120 mg.kg-1)。各组又分为缺血2 h再灌注后3,6,12,24,48,72 h组,每组6只。ig给药7 d,每天1次,第7天ig 2 h后线栓法制作大脑中动脉阻断(MCAO)再灌注模型。免疫组化法检测VEGF的表达,同时评价大鼠的神经功能缺失程度。结果:与假手术组比较,缺血再灌注组大鼠出现严重的神经功能缺失症状,各时间点(3,6,12,24,48,72 h)VEGF表达增强(P<0.05,P<0.01);与缺血再灌注组比较,参芎化瘀胶囊预处理组能显著改善大鼠神经功能缺失症状,各时间点(3,6,12,24,48,72 h)VEGF表达均明显增强(P<0.05,P<0.01),其中以高剂量组效果最为显著。结论:参芎化瘀胶囊预处理对脑缺血再灌注损伤具有保护作用,其作用机制可能与增加VEGF的表达有关。
Objective: To observe the effect of Shenxionghuayu capsule preconditioning on the expression of vascular endothelial growth factor (VEGF) after cerebral ischemia-reperfusion injury in rats and to explore the effect of Shenxionghuayu capsule on acute cerebral ischemia-reperfusion Damage protection mechanism. Methods: The rats were randomly divided into sham operation group, ischemia-reperfusion group and Shenxionghuayu capsule high, medium and low dose pretreatment group (480, 240, 120 mg.kg-1). Each group was divided into 2 hours after ischemia 2 hours 3,6,12,24,48,72 h after reperfusion group, 6 in each group. ig administration for 7 days, once a day, on the seventh day after ig 2 h, the model of middle cerebral artery occlusion (MCAO) reperfusion was established. Immunohistochemistry was used to detect the expression of VEGF, meanwhile, the extent of neurological deficit in rats was evaluated. Results: Compared with the sham-operation group, the rats with ischemia-reperfusion injury developed severe neurological deficits. The expression of VEGF increased at each time point (3, 6, 12, 24, 48 and 72 h) (P < 0.01). Compared with ischemia-reperfusion group, Shenxionghuayu capsule preconditioning group could significantly improve the symptoms of neurological deficit in rats, and the expression of VEGF at each time point (3, 6, 12, 24, 48 and 72 h) (P <0.05, P <0.01), of which the high dose group was the most effective. Conclusion: Shenxionghuayu capsule preconditioning has a protective effect on cerebral ischemia-reperfusion injury, and its mechanism may be related to increasing the expression of VEGF.