替米沙坦
乳酸脱氢酶
血管紧张素II
污渍
分子生物学
化学
巨噬细胞
活力测定
单核细胞
药理学
酶
细胞
生物
生物化学
受体
内分泌学
免疫学
体外
基因
血压
作者
Z-J Shen,Cang‐Bao Xu,Li Yp,J Li,Xu Jj,Pu Xia
出处
期刊:PubMed
日期:2018-11-01
卷期号:22 (22): 8004-8012
被引量:3
标识
DOI:10.26355/eurrev_201811_16429
摘要
To investigate the effects of telmisartan on matrix metalloproteinase-9 (MMP-9) expression in macrophages induced by angiotensin II (Ang II) and its mechanism.THP-1 cells were adopted for research, and phorbol-12-myristate-13-acetate (PMA) was utilized to induce THP-1 cells to be transformed into macrophages, with Ang II as a stimulating factor and telmisartan as a therapeutic drug. Cell counting kit-8 (CCK8) and lactate dehydrogenase (LDH) were applied to detect cell viability and toxicity. Enzyme-linked immunosorbent assay (ELISA) was performed to measure the MMP-9 release level. Polymerase Chain Reaction (PCR) and Western blotting were conducted to detect the expressions of MMP-9 messenger ribonucleic acid (mRNA) and protein, respectively. The mechanism of action was further studied, and the activity of cyclooxygenase-2 (COX2)/macrophage-expressed gene 1 (mPEG1) pathway was determined via PCR and Western blotting.The 1 mM Ang II could remarkably activate the synthesis and release of MMP-9 as well as the COX2/mPEG1 pathway in macrophages. However, telmisartan could effectively repress the Ang II-induced MMP-9 synthesis and release in the macrophages, and suppress the COX2/mPEG1 pathway in the macrophages activated by Ang II.Telmisartan can inhibit the activation of MMP-9 in the macrophages by suppressing the COX2/mPEG1 pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI