标题:Protective effect of diminazene attenuates myocardial infarction in rats via increased inflammation and ACE2 activity
作者:Chen, Junjiang; Cui, Lianqun; Yuan, Jingliang; Zhang, Songcun; Ma, Rongmei; Sang, Hongjun; Liu, Qingjiang; Shan, Lianfeng
作者机构:[Chen, Junjiang] Shandong Univ, Sch Med, Jinan 250100, Shandong, Peoples R China.; [Cui, Lianqun] Shandong Univ, Shandong Prov Hosp, Dept Cardiol, J 更多
通讯作者:Cui, LQ
通讯作者地址:[Cui, LQ]Shandong Univ, Shandong Prov Hosp, Dept Cardiol, Jinan 250021, Shandong, Peoples R China.
来源:MOLECULAR MEDICINE REPORTS
出版年:2017
卷:16
期:4
页码:4791-4796
DOI:10.3892/mmr.2017.7152
关键词:diminazene; myocardial infarction; inflammation; ACE2; AT1R; MasR
摘要:The present study aimed to investigate whether diminazene attenuates myocardial infarction (MI) in rats. In addition, the present study investigated whether ACE2 signaling was involved in the effects of diminazene on protein function. A rat model of acute myocardial infarction (AMI) was established by occlusion of the left anterior descending coronary artery. The AMI model rats received intraperitoneal injections of diminazene (5 mg/kg/day) for 3 days. Treatment with diminazene significantly inhibited the expression of casein kinase and lactate dehydrogenase, and reduced infarct size in AMI rats. The findings indicated that diminazene significantly reduced the levels of inflammatory factors including tumor necrosis factor-a and interleukin-6, suppressed the protein expression of cytochrome c oxidase subunit 2 (COX-2) and inducible nitric oxide synthase (iNOS), and activated angiotensin-converting enzyme 2 (ACE2), angiotensin II receptor type 1 (AT1R) and MAS1 proto-oncogene, G protein-coupled receptor (MasR) protein expression in AMI model rats. In conclusion, the present study demonstrated that diminazene attenuated AMI in rats via suppression of inflammation, reduction of COX-2 and iNOS expression, and activation of the ACE2/AT1R/MasR signaling pathway.
收录类别:SCOPUS;SCIE
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85028705709&doi=10.3892%2fmmr.2017.7152&partnerID=40&md5=3596d44773967001222657221826483b
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