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作 者:王建萍[1,2] 刘瑞华[3] 李忠臣 张秀珍[3] 王新贤 关广聚[1]
机构地区:[1]山东大学第二医院肾内科,济南250033 [2]烟台毓璜顶医院血液净化中心,山东烟台264000 [3]烟台毓璜顶医院超声科,山东烟台264000 [4]烟台市市直机关医院,山东烟台264000
出 处:《山东大学学报(医学版)》2012年第10期68-72,共5页Journal of Shandong University:Health Sciences
摘 要:目的应用肠系膜上动脉以上部位结扎腹主动脉建立左心室肥厚大鼠模型,观察奥美沙坦对腹主动脉结扎大鼠肾脏损害的保护作用。方法 Wistar大鼠随机分为假手术组(n=13)和手术组(n=26),术后10 d将手术组大鼠随机分为模型组及奥美沙坦组[1 mg/(kg·d)灌胃]。连续治疗7周后,进行彩色超声心动图检查模型组大鼠存在左心室肥厚,奥美沙坦组左心室壁厚度同假手术组,随后进行肾脏多普勒超声检查,观察肾脏病变。应用ELISA方法观察血浆和肾脏血管紧张素Ⅱ(AngⅡ)的变化,肾脏组织行Masson染色观察大鼠肾脏胶原纤维沉积情况,采用免疫组化方法检测Bax、Bcl-2、Caspase-3蛋白的表达。结果奥美沙坦组与模型组相比肾实质回声无增强,肾动脉阻力指数降低。应用奥美沙坦药物干预后,腹主动脉结扎大鼠肾脏AngⅡ水平显著降低,肾小管间质纤维化病变消失,且能抑制Bax、Bcl-2、Caspase-3蛋白在肾小管上皮细胞中的表达。结论腹主动脉结扎导致模型组大鼠肾间质纤维化,奥美沙坦可能通过抑制肾脏局部AngⅡ的生成和调控凋亡途径起到肾脏保护作用。Objective To establish the rat model with left ventricular hypertrophy by coarctation of abdominal aorta a- bove superior mesenteric artery and to evaluate protective effects of olmesartan on kidney injuries. Methods Wistar rats were randomly divided into sham-operated group( n = 13 ) and operating group( n = 26). Then the surgical rats were subdivided into olmesartan-treated group ( 1 mg/kg ·d) ) and hypertension (HTN) group. Seven weeks after treat- ments, left ventricular hypertrophy and kidney injuries were analyzed in vivo by M-mode echocardiography and ultra- sonography respectively. Angiotensin Ⅱ ( Ang Ⅱ ) in plasma and renal tissue was observed by ELISA method. Morpho- logic features and collagen deposition in kidneys were examined by Masson staining. Expressions of Bax, Bcl-2 and Caspase-3 were evaluated by immunohistochemistry. Results Compared with HTN group, renal parenchymal echoge- nicity was unchanged and renal vascular resistive index was lower in olmesartan group by doppler ultrasound examination. Moreover olmesartan significantly decreased AngⅡ in the renal local tissue, prevented formation of tubulointersti- tial fibrosis and inhibited the expressions of Bax, Bcl-2 and Caspase-3 proteins. Conclusion Olmesartan is able to pro- tect kidney against the injury induced by abdominal aortic banding, which might due to decreased expression of AngⅡ in kidney and the inhibition of apoptosis pathway.
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