کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9296427 | 1596779 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Epigallocatechin-3-gallate, a green-tea polyphenol, suppresses Rho signaling in TWNT-4 human hepatic stellate cells
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کلمات کلیدی
HSC5-bromo-2′-deoxy-uridinePDGFLPAFCSPAGEEpigallocatechin-3-gallateFAKEGCGα-SMAPBSJnkSDSDMEMGTPMAPK - MAPKDulbecco’s modified Eagle medium - Modified Eagle اصلاح شده DulbeccoEDTA - اتیلن دی آمین تترا استیک اسید ethylenediaminetetraacetate - اتیلنیدامین تتراسیتpolyacrylamide-gel electrophoresis - الکتروفورز پلی آکریل آمید ژلBrdU - بروموداکسی اوریدینGDP - تولید ناخالص ملیTUNEL - تونلsodium dodecyl sulfate - سدیم دودسیل سولفاتHepatic stellate cell - سلول ستاره ای کبدیplatelet-derived growth factor - فاکتور رشد حاصل از پلاکتphosphate-buffered saline solution - محلول نمک فسفات بافرmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenfocal adhesion kinase - کیناز چسبندگی کانونیGuanosine triphosphate - گوانوزین تری فسفاتguanosine diphosphate - گوانوزین دی فسفاتRock - یا راک
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Epigallocatechin-3-gallate (EGCG), a major constituent of the polyphenoids in green tea, has been reported to possess a wide range of biologic activities, including antifibrogenesis. Activated hepatic stellate cells (HSCs) are central to hepatic fibrosis, and Rho (a small GTPase)-signaling pathways have been implicated in the activation and proliferation of HSCs. In this study, we investigated the effect of EGCG on Rho-signaling pathways in activated human HSC-derived TWNT-4 cells. EGCG inhibited stress-fiber formation, an indicator of Rho activation, and changed the distribution of α-smooth-muscle actin. These inhibitory effects of EGCG were restored by overexpression of constitutively active Rho. A pull-down assay revealed that activated Rho (GTP-bound state) was strongly inhibited by ECGC and accompanied by suppressed phosphorylation of focal adhesion kinase, which is a regulator of Rho-signaling pathways. 5-Bromo-2â²-deoxy-uridine incorporation demonstrated that ECGC (100 μmol/L suppressed cell growth by 80%, and terminal deoxynucleotidyl transferase viotin-deoxyruidine triphosphate nick end-labeling revealed that EGCG (100 μmol/L) caused apoptosis in half of the total cells. EGCG also strongly inhibited lysophoaphatidic acid (an activator of Rho) and induced phosphorylation of mitogen-activated protein kinases (Erk1/2, c-jun kinase, and p38). These findings demonstrate that EGCG regulates the structure and growth of HSCs by way of Rho-signaling pathways and suggest that EGCG has therapeutic potential in the setting of liver fibrosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Laboratory and Clinical Medicine - Volume 145, Issue 6, June 2005, Pages 316-322
Journal: Journal of Laboratory and Clinical Medicine - Volume 145, Issue 6, June 2005, Pages 316-322
نویسندگان
Nobuhiko Higashi, Motoyuki Kohjima, Marie Fukushima, Satoshi Ohta, Kazuhiro Kotoh, Munechika Enjoji, Naoya Kobayashi, Makoto Nakamuta,