Atractylenolide I restores HO-1 expression and inhibits Ox-LDL-induced VSMCs proliferation, migration and inflammatory responses in vitro

被引：116

作者：

Li, Weifeng ^{[1
]}

Zhi, Wenbing ^{[1
]}

Liu, Fang ^{[1
]}

He, Zehong ^{[1
]}

Wang, Xiuei ^{[1
]}

Niu, Xiaofeng ^{[1
]}

机构：

[1] Xi An Jiao Tong Univ, Sch Pharm, Xian 710061, Peoples R China

来源：

EXPERIMENTAL CELL RESEARCH | 2017年 / 353卷 / 01期

关键词：

Atractylenolide I; Atherosclerosis; Vascular smooth muscle cells; Proliferation; Migration; Inflammation; SMOOTH-MUSCLE-CELLS; NF-KAPPA-B; ATRACTYLODES-MACROCEPHALA KOIDZ; HEME OXYGENASE-1; ANGIOTENSIN-II; SIGNALING PATHWAYS; LESION FORMATION; RAW264.7; CELLS; FOAM CELLS; TNF-ALPHA;

D O I：

10.1016/j.yexcr.2017.02.040

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Pathogenesis of atherosclerosis is characterized by the proliferation and migration of vascular smooth muscle cells (VSMCs) and inflammatory lesions. The aim of this study is to elucidate the effect of atractylenolide I (AO-I) on smooth muscle cell inflammation, proliferation and migration induced by oxidized modified low density lipoprotein (Ox-LDL). Here, We found that atractylenolide I inhibited Ox-LDL-induced VSMCs proliferation and migration in a dose-dependent manner, and decreased the production of inflammatory cytokines and the expression of monocyte chemoattractant protein-1 (MCP-1) in VSMCs. The study also identified that AO-I prominently inhibited p38-MAPK and NF-kappa 3 activation. More importantly, the specific heme oxygenase-1(HO-1) inhibitor zinc protoporphyrin (ZnPP) IX partially abolished the beneficial effects of atractylenolide I on OxLDL-induced VSMCs. Furthermore, atractylenolide I blocked the foam cell formation in macrophages induced by Ox-LDL. In summary, inhibitory roles of AO-I in VSMCs proliferation and migration, lipid peroxidation and subsequent inflammatory responses might contribute to the anti-atherosclerotic property of AO-I.

引用

页码：26 / 34

页数：9

共 59 条

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