Anti-inflammatory Effects of Oleanolic Acid on LPS-Induced Inflammation In Vitro and In Vivo

被引:134
|
作者
Lee, Wonhwa [1 ,2 ]
Yang, Eun-Ju [3 ]
Ku, Sae-Kwang [4 ]
Song, Kyung-Sik [1 ]
Bae, Jong-Sup [1 ]
机构
[1] Kyungpook Natl Univ, Coll Pharm, Pharmaceut Sci Res Inst, Taegu 702701, South Korea
[2] Kyungpook Natl Univ, Dept Biochem & Cell Biol, Sch Med, Taegu 702701, South Korea
[3] Kyungpook Natl Univ, Res Team Developing Funct Hlth Food Mat BK21, Taegu 702701, South Korea
[4] Daegu Haany Univ, Dept Anat & Histol, Coll Oriental Med, Gyongsan 712715, South Korea
基金
新加坡国家研究基金会;
关键词
oleanolic acid; lipopolysaccharide; endothelium; inflammation; barrier integrity; CELL-ADHESION MOLECULE-1; TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; KOREAN MISTLETOE LECTIN; ENDOTHELIAL-CELLS; LEUKOCYTE ADHESION; E-SELECTIN; EXPRESSION; ACTIVATION; INHIBITION;
D O I
10.1007/s10753-012-9523-9
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oleanolic acid (OA) is a triterpenoid known for its anti-inflammatory and anti-cancer properties; however, the anti-inflammatory effects of OA on lipopolysaccharide (LPS)-mediated pro-inflammatory responses have not been studied. Here, we first investigated the possible anti-inflammatory effects of OA against pro-inflammatory responses in human umbilical vein endothelial cells (HUVECs) induced by LPS and the associated signaling pathways. We found that OA inhibited LPS-induced barrier disruption, expression of cell adhesion molecules (CAMs), and adhesion/transendothelial migration of monocytes to HUVECs. OA also suppressed acetic acid-induced hyperpermeability and carboxymethylcellulose-induced leukocyte migration in vivo. Further studies revealed that OA suppressed the production of tumor necrosis factor-alpha and activation of nuclear factor-kappa B by LPS. Collectively, these results suggest that OA has anti-inflammatory effects by inhibiting hyperpermeability, the expression of CAMs, and the adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapeutic agent for vascular inflammatory diseases.
引用
收藏
页码:94 / 102
页数:9
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