Protective effects of (-)-epigallocatechin-3-gallate against TNF-α-induced lung inflammation via ROS-dependent ICAM-1 inhibition

I-Ta Lee, Chih Chung Lin, Chi Yin Lee, Pei Wen Hsieh, Chuen Mao Yang

研究成果: 雜誌貢獻文章

49 引文 斯高帕斯(Scopus)

摘要

Oxidative stresses are considered to play an important role in the induction of cell adhesion molecules and proinflammatory cytokines implicated in inflammatory processes. Heme oxygenase (HO)-1 and suppressors of cytokine signaling (SOCS)-3 exert several biological functions, including antiapoptotic and anti-inflammatory effects. Here, we report that HO-1 and SOCS-3 were induced in A549 cells and human pulmonary alveolar epithelial cells (HPAEpiCs) treated with (-)-epigallocatechin-3-gallate (EGCG). EGCG protected against tumor necrosis factor (TNF)-α-mediated lung inflammation by down-regulation of oxidative stress and intercellular adhesion molecule (ICAM)-1 expression in A549 cells or HPAEpiCs and the lungs of mice. EGCG inhibited TNF-α-induced ICAM-1 expression, THP-1 cells adherence, pulmonary hematoma and leukocyte (eosinophils and neutrophils) count in bronchoalveolar lavage fluid in mice. In addition, EGCG also attenuated TNF-α-induced oxidative stress, p47phox translocation, MAPKs activation, and STAT-3 and activating transcription factor (ATF)2 phosphorylation. EGCG also reduced the formation of a TNFR1/TRAF2/Rac1/p47phox complex. Moreover, in this study, the observed suppression of TNF-α-stimulated ICAM-1 expression and reactive oxygen species (ROS) generation by EGCG was abrogated by transfection with siRNA of SOCS-3 or HO-1. These results suggested that HO-1 or SOCS-3 functions as a suppressor of TNF-α signaling, not only by inhibiting adhesion molecules expression but also by diminishing intracellular ROS production and STAT-3 and ATF2 activation in A549 cells or HPAEpiCs and the lungs of mice.
原文英語
頁(從 - 到)124-136
頁數13
期刊Journal of Nutritional Biochemistry
24
發行號1
DOIs
出版狀態已發佈 - 一月 1 2013
對外發佈Yes

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Molecular Biology
  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

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