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作 者:隆琦[1] 王骏[1] 张文[1] 王伟铭[1] 赵彩霞[1] 陈楠[1]
机构地区:[1]上海交通大学医学院附属瑞金医院肾脏科,上海200025
出 处:《中国中西医结合肾病杂志》2010年第8期669-672,753,754,共6页Chinese Journal of Integrated Traditional and Western Nephrology
基 金:上海市卫生局重点学科基金资助项目(No.5IIIO01);上海市重点学科建设基金资助项目(No.T0201);上海市领军人才基金资助项目;上海市科委重点项目(No.07JC14037)
摘 要:目的:探讨在缺血再灌注(ischemia/reperfusion,I/R)模拟急性肾损伤的大鼠模型中间质血管损伤状况及其病变机制。方法:按随机分组将15只SD大鼠分为假手术组(sham)、肾缺血再灌注损伤(I/R)6 h组、24 h组,每组5只,测定血尿素氮水平,并观察肾脏病理改变;免疫组织化学法观察巨噬细胞浸润、促血管生成因子-血管内皮生长因子(VEGF)的表达,免疫荧光法检测肾小管间质血管的分布,原位缺口末端标记法(TUNEL)检测肾小管上皮细胞凋亡。结果:I/R 6 h、24 h组与sham组相比,BUN明显升高(P<0.05),巨噬细胞浸润明显(P<0.05),VEGF表达量下降,间质血管密度下降(P<0.05),上皮细胞凋亡增多(P<0.05)。结论:I/R损伤后炎症细反应所致间质血管密度降低是肾小管上皮细胞损伤的重要机制。Objective:To observe the effects of ischemia reperfusion injury on peritubular capillary desnity and to investigate the relationship between peritubular capillary and vascular endothelia growth factor(VEGF) expression,macrophage infiltration in the rat renal tissue.Methods:Male Sprague Dawley rats(weight:200±20 g) were randomized to two groups:ischemia-reperfusion injury group and sham operation group.The rats were sacrificed at 6,24 h after reperfusion.Blood urea nitrogen(BUN) and serum creatinine(Scr) levels were measured.The pathologic change was detected by PAS.Macrophage infiltration and VEGF expression were detected by immunohistochemistry(IHC) staining.The tubular epithelial cells' apoptosis was detected by double staining of lectin and Terminal deoxynucleotidy transferase dUTP nick end labeling.Peritubular capillary endothelia cells were labeled with reca and the peritubular capillary density was calculated.Results:BUN level increased significantly after ischemia-reperfusion injury between two groups.Obvious tubular injury of IRI group was observed with PAS staining.IHC staining showed obvious macrophage infiltration which located around renal tubules and glomerulus.Progressive macrophage infiltration was correlated with diminished VEGF express.Peritubular capillary density is decreased in I/R rat compared to sham operation group.Conclusion:a) Peritubular capillary injury plays an important role in the pathogenesis of IRI;b) Macrophage may inhibit the production of VEGF and induce the decrease of peritubular capillary density.
关 键 词:肾缺血再灌注 管周毛细血管网炎症反应
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