کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8337512 | 1540677 | 2013 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Protective effects of (â)-epigallocatechin-3-gallate against TNF-α-induced lung inflammation via ROS-dependent ICAM-1 inhibition
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کلمات کلیدی
DPISOCSEGCGATFBAL(−)-Epigallocatechin-3-gallate - (-) - Epigallocatechin-3-gallateapo - آپوApocynin - آپوسیینینLung inflammation - التهاب ریهNADPH oxidase - اکسیداز NADPH diphenyleneiodonium chloride - دی فینیلنیدونیم کلریدCytokines - سیتوکین هاactivating transcription factor - فعال کردن عامل رونویسیbronchoalveolar lavage - لارو برونکلو آلوئولارcarbon monoxide - منوکسیدکربنheme oxygenase - همگام اکسژنازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Protective effects of (â)-epigallocatechin-3-gallate against TNF-α-induced lung inflammation via ROS-dependent ICAM-1 inhibition Protective effects of (â)-epigallocatechin-3-gallate against TNF-α-induced lung inflammation via ROS-dependent ICAM-1 inhibition](/preview/png/8337512.png)
چکیده انگلیسی
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 (â)-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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Nutritional Biochemistry - Volume 24, Issue 1, January 2013, Pages 124-136
Journal: The Journal of Nutritional Biochemistry - Volume 24, Issue 1, January 2013, Pages 124-136
نویسندگان
I-Ta Lee, Chih-Chung Lin, Chi-Yin Lee, Pei-Wen Hsieh, Chuen-Mao Yang,