TY - JOUR
T1 - Resveratrol attenuates HMGB1 signaling and inflammation in house dust mite-induced atopic dermatitis in mice
AU - Karuppagounder, Vengadeshprabhu
AU - Arumugam, Somasundaram
AU - Thandavarayan, Rajarajan A.
AU - Pitchaimani, Vigneshwaran
AU - Sreedhar, Remya
AU - Afrin, Rejina
AU - Harima, Meilei
AU - Suzuki, Hiroshi
AU - Nomoto, Mayumi
AU - Miyashita, Shizuka
AU - Suzuki, Kenji
AU - Watanabe, Kenichi
N1 - Publisher Copyright:
© 2014 Elsevier B.V. All rights reserved.
PY - 2014/12
Y1 - 2014/12
N2 - Resveratrol is a polyphenol abundantly found in red grape skin and is effective against antiaging and antiinflammation associated with immune responses. In this study, we have investigated the effect of resveratrol on skin lesion, high mobility group box (HMGB)1 and inflammation pathway in an atopic dermatitis (AD) mouse model. AD-like lesion was induced by the application of house dust mite extract to the dorsal skin of NC/Nga mouse. After AD induction, resveratrol (20 mg/kg, p.o.) was administered daily for 2 weeks. We evaluated dermatitis severity, histopathological changes, serum levels of T helper (Th) cytokines (interferon (IFN)γ, interleukin (IL)-4) and changes in protein expression by Western blotting for HMGB1, receptor for advanced glycation end products (RAGE), toll like receptor (TLR)4, nuclear factor (NF)κB, phosphatidylinositide 3-kinase (PI3K), extracellular signal-regulated kinase (ERK)1/2, cyclooxygenase (COX)2, tumor necrosis factor (TNF)α, IL-1β, IL-2Rα and other inflammatory markers in the skin of AD mice. Treatment of resveratrol inhibited the development of the AD-like skin lesions. Histological analysis showed that resveratrol inhibited hypertrophy, intracellular edema, mast cells and infiltration of in flammatory cells. Furthermore, resveratrol treatment down-regulated HMGB1, RAGE, p-NFκB, p-PI3K, p-ERK1/2, COX2, TNFα, IL-1β, IL-2Rα, IFNγ and IL-4. Considering all these findings together, the HMGB1 pathway might be a potential therapeutic target in skin inflammation, and resveratrol treatment could have beneficial effects on AD by modulating the HMGB1 protein expression.
AB - Resveratrol is a polyphenol abundantly found in red grape skin and is effective against antiaging and antiinflammation associated with immune responses. In this study, we have investigated the effect of resveratrol on skin lesion, high mobility group box (HMGB)1 and inflammation pathway in an atopic dermatitis (AD) mouse model. AD-like lesion was induced by the application of house dust mite extract to the dorsal skin of NC/Nga mouse. After AD induction, resveratrol (20 mg/kg, p.o.) was administered daily for 2 weeks. We evaluated dermatitis severity, histopathological changes, serum levels of T helper (Th) cytokines (interferon (IFN)γ, interleukin (IL)-4) and changes in protein expression by Western blotting for HMGB1, receptor for advanced glycation end products (RAGE), toll like receptor (TLR)4, nuclear factor (NF)κB, phosphatidylinositide 3-kinase (PI3K), extracellular signal-regulated kinase (ERK)1/2, cyclooxygenase (COX)2, tumor necrosis factor (TNF)α, IL-1β, IL-2Rα and other inflammatory markers in the skin of AD mice. Treatment of resveratrol inhibited the development of the AD-like skin lesions. Histological analysis showed that resveratrol inhibited hypertrophy, intracellular edema, mast cells and infiltration of in flammatory cells. Furthermore, resveratrol treatment down-regulated HMGB1, RAGE, p-NFκB, p-PI3K, p-ERK1/2, COX2, TNFα, IL-1β, IL-2Rα, IFNγ and IL-4. Considering all these findings together, the HMGB1 pathway might be a potential therapeutic target in skin inflammation, and resveratrol treatment could have beneficial effects on AD by modulating the HMGB1 protein expression.
KW - Cytokine
KW - High mobility group box protein 1
KW - Inflammation
KW - Nuclear factor kappa b
KW - Receptor for advanced glycation end products
KW - Resveratrol
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U2 - 10.1016/j.intimp.2014.10.014
DO - 10.1016/j.intimp.2014.10.014
M3 - Article
C2 - 25466270
AN - SCOPUS:84912097756
VL - 23
SP - 617
EP - 623
JO - International Immunopharmacology
JF - International Immunopharmacology
SN - 1567-5769
IS - 2
ER -