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作 者:蒋跃绒[1] 殷惠军[1] 刘颖[1] 陈可冀[1]
出 处:《中国中西医结合杂志》2008年第10期921-924,共4页Chinese Journal of Integrated Traditional and Western Medicine
基 金:国家自然科学基金项目(No.90409021)
摘 要:目的观察赤芍801对急性心肌梗死大鼠血清炎症因子IL-1β、TNF-α及缺血心肌环氧合酶-2(COX-2)、细胞间黏附分子-1(ICAM-1)蛋白表达的影响。方法结扎冠脉左前降支造成大鼠急性心肌梗死模型,以标准肢体导联Ⅱ心电图ST段弓背抬高示AMI形成。大鼠随机分为6组:正常对照组、假手术组、模型组、赤芍801大剂量组(80mg·kg-1.d-1,腹腔注射)、赤芍801小剂量组(40mg·kg-1.d-1,腹腔注射)、阿司匹林对照组(25mg·kg-1.d-1,灌胃),共给药7天。放免法检测血清IL-1β、TNF-α含量,免疫组化法检测心肌组织COX-2、ICAM-1表达。结果与假手术组比较,模型组TNF-α水平明显升高(P<0.05),但IL-1β水平无明显升高。与假手术组比较,模型组缺血区心肌组织COX-2、ICAM-1表达升高(P<0.05)。与模型组比较,赤芍801小剂量组可降低血清TNF-α水平,并抑制缺血心肌组织COX-2、ICAM-1表达。结论赤芍801小剂量组可减轻急性心肌梗死大鼠血清炎症因子TNF-α水平,抑制缺血心肌组织COX-2、ICAM-1表达。Objective To investigate the effects of Propyl Gallate (PrG) on serum inflammatory factors and protein expression of cyclooxygenase-2 (COX-2) and intercellular adhesion molecule-1 ( ICAM-1 ) in ischemic myocardium of rats with acute myocardial infarction (AMI). Methods AMI model was induced by ligating the left anterior descending (LAD) branch of coronary artery in Wistar rats, and the perfect modeling was certified with ST segment elevation by standard limb lead Ⅱ of electrocardiogram. Rats were randomly divided into 6 groups : Group A of normal rats, Group B of rats through sham operation, Group C of AMI model rats, Group D of model rats treated with high dose PrG (80 mg · kg^-1 · d^-1 , via peritoneal injection) , Group E of model rats treated with low dose PrG (40 mg · kg^-1 · d^-1, via peritoneal injection) , and Group F of model rats treated with aspirin (25 mg · kg^-1 · d^-1, via gastrogavage) , all the treatments were given in succession for 7 days. Radioimmunoassay (RIA) was used to determine serum contents of interleukin (IL) -1β and tumor necrosis factor-α (TNF-α) , immunohistoehemistry was used to determine the level of COX-2 and ICAM-1 protein expression in myocardium. Results Compared with Group B, the serum level of TNF-α increased significantly, but not the level of IL-1β in Group C. Besides, the COX-2 and ICAM-1 protein expressions in ischemic myoeardium increased in Group C. All the above-mentioned changes were reversed to certain extent in Group E after treatment. Conclusions PrG (40 mg· kg^-1 · d^-1 ) could decrease the serum level of inflammatory factor TNF-α, and slightly inhibit COX-2 and ICAM-1 protein expression in ischemie myoeardium of AMI rats.
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