摘要
目的:探讨复方血竭胶囊(CXJC)对大鼠局灶性脑缺血-再灌注后脑组织中超氧化物歧化酶(SOD)、丙二醛(MDA)含量和细胞间粘附分子(ICAM-1)表达的影响。方法:雄性SD大鼠40只,随机分为假手术组、缺血再灌组、CXJC低剂量组(0.14 g.kg-1)、CXJC中剂量组(0.56 g.kg-1)、CXJC高剂量组(1.12 g.kg-1),每组8只。采用尼龙线大鼠大脑中动脉栓塞法造成大鼠脑缺血再灌注模型。缺血2 h再灌24 h后,采用5级评分法判定大鼠神经功能缺损、按干湿重法计算脑组织含水量、TTC染色观察梗死灶面积。采用黄嘌呤氧化酶法和硫代巴比妥酸法测定脑组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性,免疫组织化学法检测ICAM-1的表达。结果:CXJC低、中、高剂量组均降低缺血3 h时的神经症状功能缺损评分,其评分与模型组比差异显著(P<0.01);与缺血再灌组比较,CXJC0.14,0.56,1.12 g.kg-1均能明显降低脑组织MDA含量,增加脑组织SOD活性(P<0.01或P<0.05),CXJC 1.12 g.kg-1还能明显抑制ICAM-1表达的增加(P<0.01)。结论:CXJC通过清除氧自由基和抑制ICAM-1表达而发挥对脑缺血-再灌注后脑组织的保护作用。
Objective: To study the effects of Compound Xuejie capsule (CXJC) on the level of SOD, MDA and the expression of intercellular adhesion molecule-1 (ICAM-1) following focal cerebral ischemia-reperfusion in rats. Methods: 40 male Sprague-Dawley rats were randomly divided into: sham group, ischemia group, CXJC of a low dose group(0.14 g · kg^-1), CXJC of a middle dose group(0.56 g ·kg^-1), CCXJCof a high dose group(1.12 g · kg^-1). There were 8 animals in each group. The animal models of middle cerebral artery occlusion (MCAO) were established in rats. At 24 h after MCAO for 2 h, content changes of malondiadehyde(MDA) and superoxide dismutase (SOD), the activity of SOD and the content of MDA were measured respectively by xanthine oxidase method and thiobarbituric acid(TBA) method. The expression of ICAM-1 was observed by immunohistochemistry. Results: Compared with ischemia group, XJC 0.14,0. 56,1.12 g · kg^-1 significantly increased the activity of SOD and decrease the content of MDA in brain tissue (P〈0.01 or P〈0. 05). CXJC 1. 12 g · kg^-1 also significantly decreased the expression of ICAM-1. Conclusion: CXJC has protective effects on cerebral ischemic injury by enhancing the ability of free radicals scavenging and inhibiting ICAM-1 expression.
出处
《武汉大学学报(医学版)》
CAS
2005年第6期714-717,共4页
Medical Journal of Wuhan University
关键词
复方血竭胶囊
局灶性脑缺血
氧自由基
超氧化物歧化酶
细胞间粘附分子
Compound Xuejie Capsule
Cerebral Ischemia
Reperfusion Injury
Lipid Peroxidation
Intercellular Adhesion Molecule-1