【摘要】 目的:观察与分析心脑舒通胶囊对急性脑缺血损伤过程中能量代谢障碍、自由基损伤及炎性因子表达等关键环节的影响,探讨缺血保护作用机制。方法:健康雄性W istar大鼠60只,随机分为正常组、假手术组、模型组、心脑舒通组、西药组,共5组,每组12只。心脑舒通组灌胃给予心脑舒通混悬液,西药组给予阿司匹林加尼莫地平混悬液,正常组、假手术组及模型组均给予等量蒸馏水。术前3 d开始连续灌胃给药10 mL.kg-1,每天1次,至术后3 d共7 d。采用同种系微栓子体外注入法制备大鼠多发性脑梗死模型,缺血72 h后断头取脑,常规HE染色光镜下观察患侧海马CA1区及皮层病理学改变,免疫组化SABC法染色光镜下观察肿瘤坏死因子-α(TNF-α)及白细胞介素-1β(IL-1β)在海马CA1区及皮层的表达,采用比色法测定海马组织中Na+-K+-ATP酶活性、乳酸脱氢酶(LDH)活力、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果:心脑舒通胶囊能明显减轻急性多梗大鼠海马CA1区的病理形态改变,不同程度的减少海马CA1区及皮层神经细胞内TNF-α及IL-1β表达,显著提高海马组织中ATP酶活性(P<0.01)及LDH酶活力(P<0.01),能显著提高海马组织中SOD活性(P<0.01)、降低MDA含量(P<0.01)。结论:心脑舒通胶囊具有一定的缺血损伤保护作用,其机制与改善缺血组织的能量代谢障碍和自由基损伤,抑制炎性因子过表达,多环节阻抑和调节缺血级联反应有关。更多还原

【Abstract】 Objective: To study the effect of Xinnao Shutong capsule（XNST） on energy metabolism dysfunction,free radical injury and inflammatic factors in the course of acute cerebral ischemic damage,and try to reveal the mechanism of the protection against ischemia.Method: 60 male Wistar rats weighing 280³20 g were randomly divided into five groups: normal,sham operation,model,XNST treatment（XNST-T）,and Western medicine treatment（WM-T） group.Acute multi-infarct model in rats was induced by injecting the embolus of blood powder through the right external carotid artery（ECA） into the internal carotid artery（ICA）.At 72 hours after ischemia,morphologic change and the express of tumor necrosis factor-α（TNF-α） and interleukin -1β（IL-1β）in hippocampus CA1 section and cortex were observed,biochemical criterions including the activity of Na⁺-K⁺-ATPase,lactate dehydrogenase（LDH）,superoxide dismutase（SOD）,and the content of malondialdehyde（MDA） in hippocampus were examined.Result: The morphologic change of hippocampus and cortex in both XNST-T and WM-T groups was milder than that in model group.The activity of Na⁺-K⁺-ATPase,LDH and SOD in hippocampus were all significantly decreased in model group（P<0.01）,and elevated in XNST group（P<0.01） as well as in WM-T group（P<0.01）.The content of MDA in hippocampus was significantly increased in model group（P<0.05）,and was reduced in XNST group（P<0.05） as well as in WM-T group（P<0.01）.Conclusion: The results reveal that XNST has the protective effect against cerebral ischemic injury.And its possible mechanism is that XNST can prevent the upper pathological process.更多还原