Tannic acid modulates NFκB signaling pathway and skin inflammation in NC/Nga mice through PPARγ expression

被引:61
作者
Karuppagounder, Vengadeshprabhu [1 ]
Arumugam, Somasundaram [1 ]
Thandavarayan, Rajarajan Amirthalingam [1 ,2 ]
Pitchaimani, Vigneshwaran [1 ]
Sreedhar, Remya [1 ]
Afrin, Rejina [1 ]
Harima, Meilei [1 ]
Suzuki, Hiroshi [1 ]
Nomoto, Mayumi [1 ]
Miyashita, Shizuka [1 ]
Suzuki, Kenji [3 ]
Nakamura, Masahiko [4 ]
Ueno, Kazuyuki [5 ]
Watanabe, Kenichi [1 ]
机构
[1] Niigata Univ Pharm & Appl Life Sci, Dept Clin Pharmacol, Fac Pharmaceut Sci, Niigata 9568603, Japan
[2] Houston Methodist Res Inst, Dept Cardiovasc Sci, Houston, TX 77030 USA
[3] Niigata Univ, Dept Gastroenterol, Grad Sch Med & Dent Sci, Niigata 9518510, Japan
[4] Yamanashi Prefectural Ctr Hosp, Dept Cardiol, Yamanashi, Yamanashi 4008506, Japan
[5] Niigata Univ Pharm & Appl Life Sci, Dept Pharmaceut Sci, Niigata 9568603, Japan
关键词
Tannic acid; Nuclear factor kappa B; Tumor necrosis factor; Cytokine; Peroxisome proliferator-activated receptor; CISPLATIN-INDUCED NEPHROTOXICITY; IMPROVES ATOPIC-DERMATITIS; HOUSE-DUST MITE; TOPICAL APPLICATION; SUPPRESSES; ACTIVATION; INHIBITOR; RELEASE; LESIONS; STRESS;
D O I
10.1016/j.cyto.2015.05.016
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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)kappa B 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)gamma, 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 IFN gamma and IL-4 were significantly down-regulated by tannic acid. Furthermore, tannic acid treatment inhibited DIE induced tumor necrosis factor (TNF)alpha, high mobility group protein (HMG)B1, receptor for advanced glycation end products (RAGE), extracellular signal-regulated kinase (ERK)1/2, NF kappa B, cyclooxygenase (COX)2, IL-1 beta and increased the protein expression of peroxisome proliferator-activated receptor (PPAR)gamma. Taken together, our results demonstrate that, DIE induced skin inflammation might be mediated through NF kappa B signaling and tannic acid may be a potential therapeutic agent for AD, which may possibly act via induction of PPAR gamma protein. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:206 / 213
页数:8
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