Inhibitory effect of exendin-4 on secretory group IIA phospholipase A2

被引:3
作者
Lee, Wonhwa [1 ,2 ]
Kwak, Soyoung [1 ]
Lee, Hyun-Shik [3 ]
Na, Dong Hee [1 ]
Lee, You-Mie [1 ]
Bae, Jong-Sup [1 ]
机构
[1] Kyungpook Natl Univ, Pharmaceut Sci Res Inst, CMRI, Coll Pharm, Taegu 702701, South Korea
[2] Kyungpook Natl Univ, Sch Med, Plus KNU Biomed Convergence Program BK21, Dept Biochem & Cell Biol, Taegu 702701, South Korea
[3] Kyungpook Natl Univ, Plus KNU Creat BioRes Grp BK21, Sch Life Sci, ABRC,CMRI, Taegu 702701, South Korea
基金
新加坡国家研究基金会;
关键词
Exendin-4; HUVEC; sPLA2-IIA; Inflammation; GLUCAGON-LIKE PEPTIDE-1; IN-VITRO; ANTITHROMBOTIC ACTIVITIES; ANTIINFLAMMATORY ACTION; SELECTIVE INHIBITOR; EXPERIMENTAL SEPSIS; ENDOTHELIAL-CELLS; GENE-EXPRESSION; HEPATOMA-CELLS; GLP-1; RECEPTOR;
D O I
10.1016/j.bbrc.2015.02.165
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Exendin-4 (EX4), a glucagon-like peptide-1 receptor agonist, has been reported to attenuate myocardial ischemia and reperfusion injury and inflammatory or oxidative responses. The expression level of secretory group IIA phospholipase A2 (sPLA2-IIA) is elevated in inflammatory diseases. Lipopolysaccharide (LPS) upregulates the expression of sPLA2-IIA in human umbilical vein endothelial cells (HUVECs). Here, EX4 was examined for its effects on the expression and activity of sPLA2-IIA in HUVECs and mice. Pre-treatment of cells or mice with EX4 inhibited LPS-induced sPLA2-IIA expression and activity. Additionally, EX4 suppressed LPS-induced activation of cytosolic phospholipase A2 (cPLA2) and extracellular signal-regulated kinase (ERK) 1/2. Therefore, these results show that EX4 inhibited LPS-induced expression of sPLA2-IIA by suppressing cPLA2 and ERK 1/2. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:650 / 654
页数:5
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