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奥美沙坦酯可逆转心肌梗死所致肾组织的肾小球硬化,且不影响肾功能。

Olmesartan medoxomil reverses glomerulosclerosis in renal tissue induced by myocardial infarction without changes in renal function.

作者信息

Lu Xiao-Mei, Jin Yu-Nan, Ma Ling

机构信息

Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning 110001, P.R. China.

出版信息

Exp Ther Med. 2014 Jul;8(1):105-109. doi: 10.3892/etm.2014.1695. Epub 2014 Apr 25.

Abstract

The aim of the present study was to investigate the effect of olmesartan medoxomil (OLM) on renal injury in mice with myocardial infarction (MI). A total of 33 male C57/BL/6 mice were divided into a sham surgery group (SHAM group), MI group (MI group) and OLM treatment group (OLM group). Experimental MI models were established in the mice of the MI and OLM groups by coronary artery ligation, and the mice in the OLM group were fed a daily dose of 10 mg/kg OLM for eight weeks. The results showed that MI induced a reduction in cardiac function and an increase in systolic blood pressure. In addition, increased periodic acid-Schiff (PAS) positive staining, combined with increased levels of angiotensin II (Ang II) in the plasma and kidneys, and increased expression levels of renin, angiotensin II type 1 receptor (AT1R) and angiotensinogen (AGT) in the kidney tissues was observed compared with those in the SHAM group. OLM treatment attenuated the injury by reducing the systolic blood pressure and PAS positive staining, and decreasing the expression levels of Ang II, renin, AT1R and AGT in the kidney compared with those in the MI group. It may be concluded that MI activates the intrarenal renin-angiotensin system and leads to glomerulosclerosis, and that OLM protects the kidney by inhibiting the effects of Ang II.

摘要

本研究旨在探讨奥美沙坦酯(OLM)对心肌梗死(MI)小鼠肾损伤的影响。将33只雄性C57/BL/6小鼠分为假手术组(SHAM组)、MI组和OLM治疗组(OLM组)。通过冠状动脉结扎在MI组和OLM组小鼠中建立实验性MI模型,OLM组小鼠每日给予10 mg/kg OLM,持续8周。结果显示,MI导致心功能降低和收缩压升高。此外,与SHAM组相比,观察到高碘酸-希夫(PAS)阳性染色增加,同时血浆和肾脏中血管紧张素II(Ang II)水平升高,肾组织中肾素、血管紧张素II 1型受体(AT1R)和血管紧张素原(AGT)表达水平增加。与MI组相比,OLM治疗通过降低收缩压和PAS阳性染色,以及降低肾脏中Ang II、肾素、AT1R和AGT的表达水平减轻了损伤。可以得出结论,MI激活肾内肾素-血管紧张素系统并导致肾小球硬化,而OLM通过抑制Ang II的作用保护肾脏。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec93/4061226/a7d8833959fe/ETM-08-01-0105-g00.jpg

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