TY - JOUR
T1 - Tannic acid modulates NFκB signaling pathway and skin inflammation in NC/Nga mice through PPARγ expression
AU - Karuppagounder, Vengadeshprabhu
AU - Arumugam, Somasundaram
AU - Thandavarayan, Rajarajan Amirthalingam
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 - Nakamura, Masahiko
AU - Ueno, Kazuyuki
AU - Watanabe, Kenichi
N1 - Funding Information:
This research was supported by Ministry of Education, Culture, Sports, Science and Technology of Japan , and by a grant from the Promotion and Mutual Aid Corporation for Private Schools, Japan (23602012 and 26460239) respectively.
Publisher Copyright:
© 2015 Elsevier Ltd.
PY - 2015/12/1
Y1 - 2015/12/1
N2 - Polyphenolic compound tannic acid, which is mainly found in grapes and green tea, is a potent antioxidant with anticarcinogenic activities. In this present study, we hypothesized that tannic acid could inhibit nuclear factor (NF)κB signaling and inflammation in atopic dermatitis (AD) NC/Nga mice. We have analyzed the effects of tannic acid on dermatitis severity, histopathology and expression of inflammatory signaling proteins in house dust mite extract induced AD mouse skin. In addition, serum levels of T helper (Th) cytokines (interferon (IFN)γ, interleukin (IL)-4) were measured by enzyme-linked immunosorbent assay. Treatment with tannic acid ameliorated the development of AD-like clinical symptoms and effectively inhibited hyperkeratosis, parakeratosis, acanthosis, mast cells and infiltration of inflammatory cells in the AD mouse skin. Serum levels of IFNγ and IL-4 were significantly down-regulated by tannic acid. Furthermore, tannic acid treatment inhibited DfE induced tumor necrosis factor (TNF)α, high mobility group protein (HMG)B1, receptor for advanced glycation end products (RAGE), extracellular signal-regulated kinase (ERK)1/2, NFκB, cyclooxygenase (COX)2, IL-1β and increased the protein expression of peroxisome proliferator-activated receptor (PPAR)γ. Taken together, our results demonstrate that, DfE induced skin inflammation might be mediated through NFκB signaling and tannic acid may be a potential therapeutic agent for AD, which may possibly act via induction of PPARγ protein.
AB - Polyphenolic compound tannic acid, which is mainly found in grapes and green tea, is a potent antioxidant with anticarcinogenic activities. In this present study, we hypothesized that tannic acid could inhibit nuclear factor (NF)κB signaling and inflammation in atopic dermatitis (AD) NC/Nga mice. We have analyzed the effects of tannic acid on dermatitis severity, histopathology and expression of inflammatory signaling proteins in house dust mite extract induced AD mouse skin. In addition, serum levels of T helper (Th) cytokines (interferon (IFN)γ, interleukin (IL)-4) were measured by enzyme-linked immunosorbent assay. Treatment with tannic acid ameliorated the development of AD-like clinical symptoms and effectively inhibited hyperkeratosis, parakeratosis, acanthosis, mast cells and infiltration of inflammatory cells in the AD mouse skin. Serum levels of IFNγ and IL-4 were significantly down-regulated by tannic acid. Furthermore, tannic acid treatment inhibited DfE induced tumor necrosis factor (TNF)α, high mobility group protein (HMG)B1, receptor for advanced glycation end products (RAGE), extracellular signal-regulated kinase (ERK)1/2, NFκB, cyclooxygenase (COX)2, IL-1β and increased the protein expression of peroxisome proliferator-activated receptor (PPAR)γ. Taken together, our results demonstrate that, DfE induced skin inflammation might be mediated through NFκB signaling and tannic acid may be a potential therapeutic agent for AD, which may possibly act via induction of PPARγ protein.
KW - Cytokine
KW - Nuclear factor kappa B
KW - Peroxisome proliferator-activated receptor
KW - Tannic acid
KW - Tumor necrosis factor
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U2 - 10.1016/j.cyto.2015.05.016
DO - 10.1016/j.cyto.2015.05.016
M3 - Article
C2 - 26049169
AN - SCOPUS:84943665175
VL - 76
SP - 206
EP - 213
JO - Cytokine
JF - Cytokine
SN - 1043-4666
IS - 2
ER -