Protocatechuic aldehyde ameliorates experimental pulmonary fibrosis by modulating HMGB1/RAGE pathway

被引:68
作者
Zhang, Liang [1 ]
Ji, Yunxia [1 ]
Kang, Zechun [1 ]
Lv, Changjun [1 ]
Jiang, Wanglin [1 ]
机构
[1] Binzhou Med Univ, Sch Pharmaceut Sci, Yantai 264003, Peoples R China
基金
中国国家自然科学基金;
关键词
High mobility group box I; Epithelial-mesenchymal transition; Pulmonary fibrosis; Protocatechuic aldehyde; Receptor for advanced glycation end-product; Fibroblast growth factor 2; GLYCATION END-PRODUCTS; RECEPTOR; INHIBITION; EXPRESSION; PROTEIN; CELLS; RAGE;
D O I
10.1016/j.taap.2015.01.001
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
An abnormal high mobility group box 1 (HMGB1) activation and a decrease in receptor for advanced glycation end-product (RAGE) play a key role in the pathogenesis of pulmonary fibrosis. Protocatechuic aldehyde (PA) is a naturally occurring compound, which is extracted from the degradation of phenolic acids. However, whether PA has anti-fibrotic functions is unknown. In this study, the effects of PA on the transforming growth factor-beta 1 (TGF-beta 1)-mediated epithelial-mesenchymal transition (EMT) in A549 cells, on the apoptosis of human type I alveolar epithelial cells (AT I), on the proliferation of human lung fibroblasts (HLF-1) in vitro, and on bleomycin (BLM)-induced pulmonary fibrosis in vivo were investigated. PA treatment resulted in a reduction of EMT in A549 cells with a decrease in vimentin and HMGB, an increase of E-cadherin and RAGE, a reduction of HLF-1 proliferation with a decrease of fibroblast growth factor 2 (FGF-2) and platelet-derived growth factor (PDGF). Apoptosis of AT I was attenuated with an increase of RAGE. PA ameliorated BLM-induced pulmonary fibrosis in rats with a reduction of histopathological scores and collagen deposition, and a lower FGF-2, PDGF, alpha-smooth muscle actin (alpha-SMA) and HMGB1 expression, whereas higher RAGE was found in ELM-instilled lungs. Through the decrease of HGMB1 and the regulation of RAGE, PA reversed the EMT, inhibited HLF-1 proliferation as well as reduced apoptosis in AT I, and prevented pulmonary fibrosis in vivo. Collectively, our results demonstrate that PA prevents experimental pulmonary fibrosis by modulating HMGB1/RAGE pathway. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:50 / 56
页数:7
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