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机构地区:[1]浙江省立同德医院心血管一科,杭州市310012
出 处:《中华全科医学》2015年第7期1065-1067,共3页Chinese Journal of General Practice
基 金:浙江省医学会临床科研资金项目(2013ZYC-A06)
摘 要:目的观察人参皂甙Rg1(GRg1)对原发性高血压大鼠(SHR)血管内皮的保护作用并采用分子生物学技术探讨过氧化酶体增生物激活受体γ(PPARγ)信号通路的活化是否与该保护作用有关。方法本研究采用SHR大鼠作为动物模型并以WKY大鼠作为阴性对照。以GRg1灌胃法分别处理SHR(SHR+GRg1)及WKY(WKY+GRg1)大鼠。处死大鼠后分离其肠系膜上动脉,采用肠系膜上动脉血管舒张试验评估血管内皮功能;收集血清标本后,分别采用硝酸还原法、显色法以及酶联免疫吸附法(ELISA)分别检测血清中一氧化氮(NO)、丙二醛(MDA)、超氧化物歧化酶(SOD)以及肿瘤坏死因子-α(TNF-α)的水平;采用Western Blot法对动脉组织内PPARγ蛋白分子表达水平进行检测。结果与WKY以及WKY+GRg1相比,SHR大鼠肠系膜上动脉血管舒张度、血清NO及SOD以及动脉组织PPARγ表达水平显著降低,同时血清MDA及TNF-α水平显著升高(P<0.05);与SHR大鼠相比,SHR+GRg1大鼠SHR大鼠肠系膜上动脉血管舒张度、血清NO及SOD以及动脉组织PPARγ表达水平显著升高,同时血清MDA及TNF-α水平显著降低(P<0.05)。结论 GRg1对自发性高血压大鼠内皮功能具有保护作用,表现为对炎症反应的抑制作用,其机制可能与通过降低血管内皮组织内氧化应激以维持内皮细胞内的PPARγ表达有关。Objective To observe the protective effect of GRgl on vascular endothelium and to investigate the possible in- volvement of PPAR gamma activation. Methods SHR rats were used and WKY rats were selected as negative control in this study. SHR and WKY rats were treated by GRgl ( SHR + GRg1 ) and WKY( WKY + GRg1 ) respectively. After the su- perior mesenteric arterials were separated from rats, the endothelium function was assessed by superior mesenteric arterial dilation assay;NO, MDA, SOD and TNF-α levels were evaluated by nitric-reductive assay, chromatography and ELISA re- spectively in collected serum samples ; expression of PPARγin arterial tissue was detected by Western blotting. Results Compared with WKY and WKY + GRg1, the vascular dilation degree, serum levels of NO and SOD and aortic PPARγ pro- tein expression were reduced significantly(P 〈 0.05 ), while the serum levels of MDA and TNF-α were significantly in- creased( P 〈 0.05 ) ; compared with SHR, however, the vascular dilation degree, serum levels of NO and SOD and aortic PPARγ expression were increased significantly ( P 〈 0.05 ), while the serum levels of MDA and TNF-α were decreased significantly(P 〈 0.05). Conclusion GRgl showed protective effect on endothelium function in SHR rats probably via suppressing inflammation in endothelium. This mechanism was supposed to associate with attenuating oxidative stress to preserving PPARγ expression in endothelium cells.
分 类 号:R544.1[医药卫生—心血管疾病] R965[医药卫生—内科学]
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