Abstract |
Glucosamine (GS) is well known for the treatment of inflam-mation. However, the mechanism and efficacy of GS for skin inflammation are unclear. The aim of this study was to evaluate the effects and mechanism of GS in the mouse 12-O-tetradecanoyl 13-acetate (TPA)-induced ear edema model. TPA-induced ear edema was evoked in ICR or transglutaminase 2 (Tgase-2) (-/-) mice. GS was administered orally (10-100 mg/kg) or topically (0.5-2.0 w/v %) prior to TPA treatment. Orally administered GS at 10 mg/kg showed a 76 or 57% reduction in ear weight or myeloperoxidase, respectively, and a decreased expression of cyclooxy-genase-2 (COX-2), NF-κB and Tgase-2 in TPA-induced ear edema by western blot and immunohistochemistry. Role of Tgase-2 in TPA ear edema is examined using Tgase-2 (-/-) mice and TPA did not induce COX-2 expression in ear of Tgase-2 (-/-) mice. These observations suggested that Tgase-2 is involved in TPA-induced COX-2 expression in the inflamed ear of mice and anti-inflammatory effects of glucosamine is mediated through suppression of Tgase-2 in TPA ear edema.
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Authors | Mi Kyung Park, Sun A Cho, Hye Ja Lee, Eun Ji Lee, June Hee Kang, You Lee Kim, Hyun Ji Kim, Seung Hyun Oh, Changsun Choi, Ho Lee, Soo Youl Kim |
Journal | Biomolecules & therapeutics
(Biomol Ther (Seoul))
Vol. 20
Issue 4
Pg. 380-5
(Jul 2012)
ISSN: 1976-9148 [Print] Korea (South) |
PMID | 24009824
(Publication Type: Journal Article)
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