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Thalidomide prevents the progression of peritoneal fibrosis in mice.


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Title: Thalidomide prevents the progression of peritoneal fibrosis in mice.
Authors: Arai, Hideyuki / Furusu, Akira / Nishino, Tomoya / Obata, Yoko / Nakazawa, Yuka / Nakazawa, Masayuki / Hirose, Misaki / Abe, Katsushige / Koji, Takehiko / Kohno, Shigeru
Issue Date: 28-Apr-2011
Publisher: The Japan Society of Histochemistry and Cytochemistry / 日本組織細胞化学会
Citation: Acta Histochemica et Cytochemica, 44(2), pp.51-60; 2011
Abstract: Thalidomide is clinically recognized as a therapeutic agent for multiple myeloma and has been known to exert anti-angiogenic actions. Recent studies have suggested the involvement of angiogenesis in the progression of peritoneal fibrosis. The present study investigated the effects of thalidomide on the development of peritoneal fibrosis induced by injection of chlorhexidine gluconate (CG) into the mouse peritoneal cavity every other day for 3 weeks. Thalidomide was given orally every day. Peritoneal tissues were dissected out 21 days after CG injection. Expression of CD31 (as a marker of endothelial cells), proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), α-smooth muscle actin (as a marker of myofibroblasts), type III collagen and transforming growth factor (TGF)-β was examined using immunohistochemistry. CG group showed thickening of the submesothelial zone and increased numbers of vessels and myofibroblasts. Large numbers of VEGF-, PCNA-, and TGF-β-positive cells were observed in the submesothelial area. Thalidomide treatment significantly ameliorated submesothelial thickening and angiogenesis, and decreased numbers of PCNA- and VEGF-expressing cells, myofibroblasts, and TGF-β-positive cells. Moreover, thalidomide attenuated peritoneal permeability for creatinine, compared to the CG group. Our results indicate the potential utility of thalidomide for preventing peritoneal fibrosis.
Keywords: PCNA / Peritoneal fibrosis / TGF-β / Thalidomide / VEGF
URI: http://hdl.handle.net/10069/25614
ISSN: 00445991
DOI: 10.1267/ahc.10030
PubMed ID: 21614166
Relational Links: http://hdl.handle.net/10069/26735
Rights: Copyright (c) 2011 By the Japan Society of Histochemistry and Cytochemistry
Type: Journal Article
Text Version: publisher
Appears in Collections:Articles in academic journal

Citable URI : http://hdl.handle.net/10069/25614

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