Effect of taxifolin glycoside on atopic dermatitis-like skin lesions in NC/Nga mice.
Increased levels of eosinphils, IgE, IL-4, 5, and 13 and pro-inflammatory factors (COX-2, iNOS) are observed in patients with atopic dermatitis (AD). Taxifolin 3-O-beta-D-glucopyranoside (TAX) from the roots of Rhododendron mucronulatum (RM) was examined to determine whether its immunomodulatory effect was applicable for treating atopic dermatitis.A total of 7 groups of NC/Nga mice with AD were treated by topical application or intraperitoneal injection of TAX for 4 weeks. Follow-up evaluations were done to assess the changes in clinical observations, eosinophil counts, and levels of IgE, cytokines, COX-2 and iNOS.In the clinical observation during the experimental period, TAX treatment significantly reduced the severity of AD-like lesions induced in NC/Nga mice. Eosinophil and IgE levels decreased after treatment of the animals with TAX. TAX may thus be associated with improvement of eosinophil-related allergic diseases. The expression of cytokines (IL-4, 5 and 13) was significantly inhibited in the TAX-treated group, suggesting that TAX might play an immunoregulatory role associated with AD. In RT-PCR, iNOS and COX-2 expression levels were reduced in the TAX-treated group. In western blotting, the expression levels of iNOS and COX-2 were also reduced in the TAX-treated group.These findings suggest that TAX is effective for the treatment of AD by preventing the production of inflammatory cytokines and by reducing skin inflammation.
Ahn
Ji Young
JY
College of Medicine, Chung-Ang University, Seoul 156-756, South Korea.
Choi
Sun Eun
SE
Jeong
Mi Sook
MS
Park
Kwan Hee
KH
Moon
Nam Ju
NJ
Joo
Seong Soo
SS
Lee
Chung Soo
CS
Choi
Young Wook
YW
Li
Kapsok
K
Lee
Mi-Kyung
MK
Lee
Min Won
MW
Seo
Seong Jun
SJ
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D051546:Cyclooxygenase 2 / Q000032:analysis; D003521:Cyclopropanes; D016207:Cytokines / Q000097:blood; D003876:Dermatitis, Atopic / Q000188:drug therapy*; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology; D005260:Female; D006027:Glycosides / Q000494:pharmacology*; D007073:Immunoglobulin E / Q000097:blood; D007249:Inflammation / Q000188:drug therapy / Q000473:pathology; D051379:Mice; D052247:Nitric Oxide Synthase Type II / Q000032:analysis; D010936:Plant Extracts / Q000494:pharmacology; D018517:Plant Roots / Q000737:chemistry; D011794:Quercetin / Q000031:analogs & derivatives* / Q000494:pharmacology; D029793:Rhododendron / Q000737:chemistry; D012867:Skin / Q000187:drug effects* / Q000473:pathology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D003521:Cyclopropanes; D016207:Cytokines; D006027:Glycosides; D010936:Plant Extracts; D007073:Immunoglobulin E; D011794:Quercetin; C003377:taxifolin; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; C029402:diphenylcyclopropenone