Astaxanthin ameliorates lung fibrosis in vivo and in vitro by preventing transdifferentiation, inhibiting proliferation, and promoting apoptosis of activated cells

被引：43

作者：

Wang, Meirong ^{[1
]}

Zhang, Jinjin ^{[1
]}

Song, Xiaodong ^{[1
]}

Liu, Wenbo ^{[1
]}

Zhang, Lixia ^{[1
]}

Wang, Xiuwen ^{[1
]}

Lv, Changjun ^{[1
]}

机构：

[1] Binzhou Med Univ, Med Res Ctr, Yantai 264003, Peoples R China

来源：

FOOD AND CHEMICAL TOXICOLOGY | 2013年 / 56卷

关键词：

Astaxanthin; Lung fibrosis; Transdifferentiation; Apoptosis; GROWTH-FACTOR; ALVEOLAR MACROPHAGES; DIFFERENTIATION; MYOFIBROBLAST; MECHANISMS; TRANSITION; RELEASE; DEATH; EMT;

D O I：

10.1016/j.fct.2013.03.004

中图分类号：

TS2 [食品工业];

学科分类号：

0832 ;

摘要：

Astaxanthin, a member of the carotenoid family, is the only known ketocarotenoid transported into the brain by transcytosis through the blood-brain barrier. However, whether astaxanthin has antifibrotic functions is unknown. In this study, we investigated the effects of astaxanthin on transforming growth factor beta 1-mediated and bleomycin-induced pulmonary fibrosis in vitro and in vivo. The results showed that astaxanthin significantly improved the structure of the alveoli and alleviated collagen deposition in vivo. Compared with the control group, the astaxanthin-treated groups exhibited downregulated protein expressions of alpha-smooth muscle actin, vimentin, hydroxyproline, and B cell lymphoma/leukemia-2 as well as upregulated protein expressions of E-cadherin and p53 in vitro and in vivo. Astaxanthin also inhibited the proliferation of activated A549 and MRC-5 cells at median inhibitory concentrations of 40 and 30 mu M, respectively. In conclusion, astaxanthin could relieve the symptoms and halt the progression of pulmonary fibrosis, partly by preventing transdifferentiation, inhibiting proliferation, and promoting apoptosis of activated cells. (C) 2013 Elsevier Ltd. All rights reserved.

引用

页码：450 / 458

页数：9

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