کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3298446 | 1209905 | 2007 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
R-spondin1, A Novel Intestinotrophic Mitogen, Ameliorates Experimental Colitis in Mice
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کلمات کلیدی
GM-CSFgranulocyte-macrophage colony–stimulating factorTNFR-spondin 1Rspo1GLPTNBSKGFSAADSSMPO - DFOTrinitrobenzene sulfonic acid - اسید سولفونیک Trinitrobenzeneinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینBrdU - بروموداکسی اوریدینbromodeoxyuridine - برومودسوویریدینSAA, Serum amyloid A - سرم آمیلوئیدDextran sulfate sodium - سولفات سدیم دکسترانKeratinocyte growth factor - عامل رشد کراتینوسیتtumor necrosis factor - فاکتور نکروز تومورmyeloperoxidase - میلوپراکسیداز glucagon-like peptide - پپتید مشابه گلوکاگون
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Background & Aims: R-spondin 1 (Rspo1) is a novel epithelial mitogen that stimulates the growth of mucosa in both the small and large intestine. Methods: We investigated the therapeutic potential of Rspo1 in ameliorating experimental colitis induced by dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) as well as nonsteroidal anti-inflammatory drug-induced colitis in interleukin (IL)-10-decifient mice. Results: Therapeutic administration of recombinant Rspo1 protein reduced the loss of body weight, diarrhea, and rectal bleeding in a mouse model of acute or chronic DSS-induced colitis. Histologic evaluation revealed that Rspo1 improved mucosal integrity in both villus and/or crypt compartments in the small intestine and colon by stimulating crypt cell growth and mucosal regeneration in DSS-treated mice. Moreover, Rspo1 significantly reduced DSS-induced myeloperoxidase activity and inhibited the overproduction of proinflammatory cytokines, including tumor necrosis factor-α, IL-1α, IL-6, interferon-γ, and granulocyte-macrophage colony-stimulating factor, in mouse intestinal tissue, indicating that Rspo1 may reduce DSS-induced inflammation by preserving the mucosal barrier function. Likewise, Rspo1 therapy also alleviated TNBS-induced interstitial inflammation and mucosal erosion in the mouse colon. Furthermore, Rspo1 substantially decreased the histopathologic severity of chronic enterocolitis by repairing crypt epithelium and simultaneously suppressing inflammatory infiltration in piroxicam-exposed IL-10â/â mice. Endogenous Rspo1 protein was localized to villus epithelium and crypt Paneth cells in mouse small intestine. Conclusions: Our results show that Rspo1 may be clinically useful in the therapeutic treatment of inflammatory bowel disease by stimulating crypt cell growth, accelerating mucosal regeneration, and restoring intestinal architecture.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 132, Issue 4, April 2007, Pages 1331-1343
Journal: Gastroenterology - Volume 132, Issue 4, April 2007, Pages 1331-1343
نویسندگان
Jingsong Zhao, Josephine de Vera, Seiko Narushima, Eric X. Beck, Servando Palencia, Pauline Shinkawa, Kyung-Ah Kim, Yi Liu, Michael D. Levy, Daniel J. Berg, Arie Abo, Walter D. Funk,