کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9245591 | 1209949 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Therapeutic potential of follistatin for colonic inflammation in mice
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کلمات کلیدی
DSSTNPTNBSTrinitrophenylTGF-βIL-10−/−Mϕ - MφTrinitrobenzene sulfonic acid - اسید سولفونیک Trinitrobenzeneinterleukin - اینترلوکینBrdU - بروموداکسی اوریدینbromodeoxyuridine - برومودسوویریدینtransforming growth factor-β - تبدیل فاکتور رشد βDigoxygenin - دیگوکسینژینLamina Propria Mononuclear Cells - سلول های تک هسته ای Lamina PropriaDIG - شماMacrophages - ماکروفاژها،درشت خوارها
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Background & Aims: Activins belong to the transforming growth factor-β superfamily. Recent studies have shown that activin and its natural antagonist, follistatin, are involved in tissue repair and inflammatory processes. The aim of this study was to determine whether neutralization of activins with follistatin would have an in vivo anti-inflammatory effect in several murine models of colitis. Methods: We assessed activin levels in the colitis induced by intracolonic administration of trinitrobenzene sulfonic acid (TNBS). We subsequently tested the effects of an intraperitoneal injection of follistatin before or after induction of TNBS colitis. We also examined the established colitis induced by oral dextran sulfate sodium (DSS) as well as the spontaneous colitis that develops in interleukin (IL)-10 gene-deficient (IL-10â/â) mice. Results: Levels of activin transcripts in the colon during the acute phase of TNBS colitis were up-regulated. Epithelial cells, infiltrating macrophages (MÏ), and endothelial cells produced excess activin βA. Pretreatment with follistatin increased the survival rate of mice with TNBS colitis from 33% to 82% and decreased the plasma levels of IL-6 and amyloid A. Administration of follistatin also reduced the histologic score and tissue myeloperoxidase activity in established TNBS and DSS colitis and reduced the severity of the colitis in IL-10â/â mice. Based on results obtained from 3 mouse models and from in vitro experiments, follistatin promoted the proliferation of colonic epithelial cells. Conclusions: Neutralization of activins by follistatin promoted epithelial cell division and tissue repair, clearly suggesting a treatment modality for intestinal inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 128, Issue 2, February 2005, Pages 411-423
Journal: Gastroenterology - Volume 128, Issue 2, February 2005, Pages 411-423
نویسندگان
Taeko Dohi, Chieko Ejima, Rie Kato, Yuki I. Kawamura, Rei Kawashima, Noriko Mizutani, Yoshiaki Tabuchi, Itaru Kojima,