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目的观察黄芪多糖(APS)对异丙肾上腺素(ISO)诱导的心肌肥厚大鼠内皮功能的保护作用及其机制。方法 ip 10 mg/kg ISO制备大鼠心肌肥厚模型,60只SD大鼠随机分为6组:对照组,模型组,APS200、400、800mg/kg组,阳性药(普萘洛尔40mg/kg)组,每组10只。各给药组连续ig给药2周,并于给药1 d后ip ISO 2周,对照组给了予等体积的生理盐水。末次给药后禁食12 h,取血,分离循环内皮细胞(CEC)并计数。检测全心质量指数(HMI)、左室质量指数(LVMI);取主动脉组织进行氢化乙啡啶(DHE)超氧阴离子染色;Western blotting法检测血管组织p65、Cu/Zn-SOD蛋白表达。结果与对照组比较,模型组HMI、LVMI分别增加了38.41%、44.91%(P<0.01),CEC数目增多(P<0.01),血管超氧阴离子生成量增加,p65蛋白表达增加,Cu/Zn-SOD蛋白表达下降(P<0.01)。与模型组比较,APS400、800mg/kg剂量组HMI、LVMI降低(P<0.05),CEC数目减少(P<0.01),血管壁超氧阴离子生成减少,p65表达下降,Cu/Zn-SOD蛋白表达升高(P<0.05、0.01)。结论 APS可能通过降低血管壁超氧阴离子生成,升高Cu/Zn-SOD表达,降低p65表达,改善血管炎症和氧化应激状态,保护心肌肥厚大鼠血管内皮功能。
Objective To observe the protective effect of astragalus polysaccharides (APS) on endothelial function in rats with isoproterenol (ISO) -induced myocardial hypertrophy and its mechanism. Methods Sixty SD rats were randomly divided into 6 groups: control group, model group, APS 200, 400, 800 mg / kg group, positive drug (propranolol 40 mg / kg ) Group, 10 in each group. Each administration group was given continuous ig administration for 2 weeks, ip 2 weeks after administration, and the control group was given an equal volume of physiological saline. Fasting for 12 h after the last administration, blood was collected, and circulating endothelial cells (CECs) were separated and counted. The whole heart mass index (HMI) and left ventricular mass index (LVMI) were measured. Aortic tissue was stained with hydrogen peroxide (DHE) and the protein expression of p65 and Cu / Zn-SOD was detected by Western blotting. Results Compared with the control group, the HMI and LVMI in model group increased by 38.41% and 44.91% (P <0.01), while the number of CEC increased (P <0.01), while the production of superoxide anion increased and the expression of p65 protein increased. -SOD protein expression decreased (P <0.01). Compared with the model group, the levels of HMI and LVMI decreased (P <0.05) and the number of CEC decreased (P <0.01), the expression of superoxide anion decreased, the expression of p65 decreased and the expression of Cu / Zn-SOD protein decreased Increased (P <0.05,0.01). Conclusions APS may protect vascular hypertrophy of vascular hypertrophy in rats by reducing the production of superoxide anion, increasing the expression of Cu / Zn-SOD, decreasing the expression of p65, improving vascular inflammation and oxidative stress.