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目的:探讨三七皂苷R1对大鼠缺血心肌VEGF、bFGF的影响。方法:选择雄性Wistar大鼠39只,建立心肌梗死(AMI)模型,术后24h存活大鼠随机分为药物组(n=13)、对照组(n=13),另设假手术组(n=8)。药物组给予三七皂苷R1水溶液(2.5 mg·kg-1·d-1)腹腔注射、对照组及假手术组给予等体积生理盐水腹腔注射,用药4周。于实验终点处死大鼠,心肌组织取材,Ⅷ因子染色计数微血管数(MVC)及微血管密度(MVD),免疫组织化学法观察缺血心肌VEGF、bFGF蛋白的表达。结果:药物组及对照组MVC、MVD均高于假手术组,且药物组高于对照组(P<0.05);大鼠缺血心肌药物组及对照组VEGF、bFGF蛋白表达均高于假手术组(P<0.05),且药物组高于对照组(P<0.05)。结论:三七皂苷R1促进大鼠缺血心肌血管再生同时可上调缺血心肌VEGF、bFGF蛋白水平。
Objective: To investigate the effect of notoginsenoside R1 on VEGF and bFGF in ischemic myocardium of rats. Methods: Thirty-nine male Wistar rats were randomly divided into three groups: drug group (n = 13), control group (n = 13) and sham operation group = 8). The drug group was given intraperitoneal injection of notoginsenoside R1 aqueous solution (2.5 mg · kg-1 · d-1), and the control group and sham-operated group were given intraperitoneal injection of equal volume of saline for 4 weeks. The rats were sacrificed at the end of the experiment, myocardial tissue samples were collected, and the number of microvessel density (MVC) and microvessel density (MVD) were calculated. The expressions of VEGF and bFGF protein in ischemic myocardium were observed by immunohistochemistry. Results: The MVC and MVD in the drug group and the control group were significantly higher than those in the sham operation group (P <0.05). The protein expressions of VEGF and bFGF in the ischemic myocardium group and the control group were significantly higher than those in the sham group Group (P <0.05), and the drug group was higher than the control group (P <0.05). Conclusion: Notoginsenoside R1 can promote the angiogenesis of ischemic myocardium and up-regulate the expression of VEGF and bFGF protein in ischemic myocardium.