卡托普利
基质金属蛋白酶
肾素-血管紧张素系统
医学
冲程(发动机)
内分泌学
金属蛋白酶
内科学
基质金属蛋白酶9
血管紧张素II
基质金属蛋白酶3
下调和上调
血压
化学
生物化学
工程类
基因
机械工程
作者
Yuying Su,Huanmin Li,Zhenxing Yan,Mingchun Li,Ji-peng Wei,Wenxia Zheng,Siqin Liu,Yi Deng,Huifang Xie,Chunguang Li
出处
期刊:Life Sciences
[Elsevier]
日期:2019-08-01
卷期号:231: 116563-116563
被引量:11
标识
DOI:10.1016/j.lfs.2019.116563
摘要
In the present study, we investigated the roles of renin-angiotensin system (RAS) activation and imbalance of matrix metalloproteinase-9 (MMP-9)/tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) in cold-induced stroke during chronic hypertension, as well as the protective effects of captopril and recombinant human TIMP-1 (rhTIMP-1). Rats were randomly assigned to sham; 2-kidney, 2-clip (2K-2C); 2K-2C + captopril, and 2K-2C + rhTIMP-1 groups. After blood pressure values had stabilized, each group was randomly divided into an acute cold exposure (ACE) group (12-h light at 22 °C/12-h dark at 4 °C) and a non-acute cold exposure (NACE) group (12-h light/12-h dark at 22 °C), each of which underwent three cycles of exposure. Captopril treatment was administered via gavage (50 mg/kg/d), while rhTIMP-1 treatment was administered via the tail vein (60 μg/kg/36 h). In the 2K-2C group, angiotensin II (AngII) and MMP-9 levels increased in both the plasma and cortex, while no such changes in TIMP-1 expression were observed. Cold exposure further upregulated AngII and MMP-9 levels and increased stroke incidence. Captopril and rhTIMP-1 treatment inhibited MMP-9 expression and activation and decreased stroke incidence in response to cold exposure. The present study is the first to demonstrate that cold exposure exacerbates imbalance between MMP-9 and TIMP-1 by activating the RAS, which may be critical in the initiation of stroke during chronic hypertension. In addition, our results suggest that captopril and rhTIMP-1 exert protective effects against cold-induced stroke by ameliorating MMP-9/TIMP-1 imbalance.
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