Journal
BIOMOLECULES & THERAPEUTICS
Volume 20, Issue 4, Pages 380-385Publisher
KOREAN SOC APPLIED PHARMACOLOGY
DOI: 10.4062/biomolther.2012.20.4.380
Keywords
Glucosamine; TPA-induced ear edema; Transglutaminase-2; Cyclooxygenase-2; NF-kappa B; Tgase-2 (-/-) mice
Funding
- National Cancer Center [NCC1110011-1]
- National Research Foundation [2010-0029919, 2011-0022074]
- Ministry of Education, Science & Technology, Korea [2011-0030173]
- National Research Foundation of Korea [2011-0030173, 2011-0022074, 2010-0029919] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Glucosamine (GS) is well known for the treatment of inflammation. 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 cyclooxygenase-2 (COX-2), NF-kappa B 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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