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C-C趋化因子受体2在盐敏感性高血压所致肾脏损害中的作用

孙邈 崔琳 刘卫红 高原 沈思 朱明军 王幼平

中国医学科学院学报2013,Vol.35Issue(1):29-35,7.
中国医学科学院学报2013,Vol.35Issue(1):29-35,7.DOI:10.3881/j.issn.1000-503X.2013.01.006

C-C趋化因子受体2在盐敏感性高血压所致肾脏损害中的作用

Role of Chemokine Receptor 2 in Renal Damage Induced by Deoxycorticosterone Acetate-salt Hypertension

孙邈 1崔琳 1刘卫红 1高原 1沈思 1朱明军 1王幼平1

作者信息

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摘要

Abstract

Objective To determine the role of chemokine receptor 2 ( CCR2) in the development of salt-sensitive hypertension-induced renal damage. Methods We investigated the renal damage induced by uninephrectomy and deoxycorticosterone acetate ( DOCA) -salt in mice treated with or without a selective CCR2 antagonist RS504393 for 4 weeks. Sham mice underwent uninephrectomy without receiving DOCA and saline. Systolic blood pressure, urinary excretion of albumin and 8-isoprostane,creatinine clearance,glomerulosclerosis,renal tubulointerstitial injury, and renal monocyte/macrophage infiltration were measured. Results DOCA-salt treatment led to increased systolic blood pressure, increased urinary excretion of albumin and 8-isoprostane, decreased creatinine clearance, glomerulosclerosis, renal tubulointerstitial injury, and renal monocyte/macrophage infiltration compared with the sham mice (P < 0. 05). All of them were prevented by CCR2 inhibition (P < 0. 05). Conclusion Blockade of CCR2 prevents renal damage induced by DOCA-salt treatment, suggesting that CCR2-mediated monocyte/macrophage infiltration may contribute to salt-sensitive hypertension-induced renal injury.

关键词

盐敏感性高血压/肾脏损害/C-C趋化因子受体2/阻断剂/单核/巨噬细胞

Key words

salt-sensitive hypertension/ renal injury/ chemokine receptor 2/ antagonist/ monocyte/macrophage

分类

医药卫生

引用本文复制引用

孙邈,崔琳,刘卫红,高原,沈思,朱明军,王幼平..C-C趋化因子受体2在盐敏感性高血压所致肾脏损害中的作用[J].中国医学科学院学报,2013,35(1):29-35,7.

基金项目

国家自然科学基金(81170243) (81170243)

中国医学科学院学报

OA北大核心CSCDCSTPCDMEDLINE

1000-503X

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