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作 者:田登科[1] 胡送友[1] 凌霜[1] 陈刚领[1] 李亚娟[1] 唐宁[1] 刘俊[1] 卞卡[1,2]
机构地区:[1]上海中医药大学穆拉德中药现代化研究中心,上海201203 [2]美国德克萨斯大学休斯顿医学院综合生物及药理学系,德克萨斯大学分子医学研究所,休斯顿tx77030
出 处:《生物物理学报》2010年第4期309-315,共7页Acta Biophysica Sinica
基 金:supported by grants from Key Projectof Ministry of Science and Technology (2006BAI11B08-03);E-Institutes of Nitric Oxide and Inflammatory Medicine of Shanghai Municipal Education Commission (E-04010);Key Project of Shanghai Committee of Science & Technology (08430711300,08DZ1972104)~~
摘 要:通过考察阿托伐他汀(atorvastatin, ATO) 对自发性高血压大鼠(spontaneously hypertensive rats, SHR) 肾脏炎性损害的影响, 探讨了 ATO 对高血压肾脏并发症的防治作用。将4周龄SHR分为高血压模型组和ATO治疗组(8mg/kg),以同周龄的Wistar-Kyoto大鼠为正常对照。灌胃给药8周后, 采用酶联免疫法(enzyme linked immunosorbent assay)测定血浆和肾组织血管紧张素Ⅱ(angiotensin, AngⅡ)含量;测定诱导性一氧化氮合酶(inducible nitric oxide synthase, iNOS)及细胞间粘附分子-1(intercellular adhesion molecule-1, ICAM-1) 的蛋白表达和亚硝酸阴离子(nitrite, NO2-)含量,以评价肾脏炎症状态; 以苏木素伊红(hematoxylin and eosin)和过碘酸六胺银染色(periodic acid-silver metheramine) 染色示SHR肾小球和肾间质形态学病变,并以尿蛋白含量为指标衡量肾脏功能。结果显示,ATO给药后显著降低了SHR肾组织 AngⅡ含量;肾组织iNOS和ICAM-1的蛋白表达及NO2-含量明显降低,同时伴随着SHR肾脏病理形态的改善和肾功能的提高。该研究表明,ATO可显著改善SHR肾脏炎性损害,ATO可能在高血压肾脏并发症的防治方面有一定的疗效。This study was designed to investigate the effect of atorvastatin (ATO) on inflammatory damage of kidney from spontaneously hypertensive rats (SHR), and to explore preventive and therapeutic usage of ATO on hypertensive nephropathy. Male SHR of 4 weeks old were divided into SHR model group and SHR+ATO group (8 mg/kg). Age-matched Wistar-Kyoto rats were used as normal control. All rats were killed at 12 wk of age. Enzyme linked immunosorbent assay (ELISA) was used to determine plasma and renal angiotensin II (AngII) contents. Renal inflammatory status was evaluated by the following parameters: inducible nitric oxide synthase (iNOS); intercellular adhesion molecule-1 (ICAM-1); plasma and renal tissue nitrite (NO2-) concentration; histological changes of glomeruli and tubuleinterstitum of the kidney. Renal function was evaluated by urinary excretion of total protein. The results showed that ATO treatment decreased renal Ang Ⅱ concentration significantly. ATO inhibited renal inflammation as reflected through reduced protein expression of iNOS and ICAM-1, decreased NO2-concentration in plasma and renal tissue. The ATO significantly improved renal function of hypertensive rats. This study indicates that ATO is a potent suppressor of renal inflammatory damage in SHR, which may serve the base for therapeutic utility of ATO in hypertensive nephropathy.
分 类 号:R544.1[医药卫生—心血管疾病] R285.5[医药卫生—内科学]
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