PMID- 26621445
OWN - NLM
STAT- MEDLINE
DCOM- 20160912
LR  - 20181202
IS  - 1793-6853 (Electronic)
IS  - 0192-415X (Linking)
VI  - 43
IP  - 8
DP  - 2015
TI  - Resveratrol Suppresses Cytokine Production Linked to FcepsilonRI-MAPK Activation in 
      IgE-Antigen Complex-Exposed Basophilic Mast Cells and Mice.
PG  - 1605-23
AB  - A complicated interplay between resident mast cells and other recruited 
      inflammatory cells contributes to the development and progression of allergic 
      inflammation entailing the promotion of T helper 2 (Th2) cytokine responses. The 
      current study examined whether resveratrol suppressed the production of 
      inflammatory Th2 cytokines in cultured rat basophilic leukemia RBL-2H3 cells. 
      Cells pre-treated with resveratrol nontoxic at 1-25 muM were sensitized with 
      anti-dinitrophenyl (anti-DNP), and subsequently stimulated by dinitrophenyl-human 
      serum albumin (DNP-HSA) antigen. Resveratrol dose-dependently diminished the 
      secretion of interleukin (IL)-3, IL-4, IL-13 as well as tumor necrosis factor 
      (TNF)-alpha by the antigen stimulation from sensitized cells. It was found that 
      resveratrol mitigated the phosphorylation of p38 MAPK, ERK, and JNK elevated in 
      mast cells exposed to Fc epsilon receptor I (FcepsilonRI)-mediated immunoglobulin E 
      (IgE)-antigen complex. The FcepsilonRI aggregation was highly enhanced on the surface 
      of mast cells following the HSA stimulation, which was retarded by treatment with 
      1-25 muM resveratrol. The IgE-receptor engagement rapidly induced tyrosine 
      phosphorylation of c-Src-related focal adhesion protein paxillin involved in the 
      cytoskeleton rearrangement. The FcepsilonRI-mediated rapid activation of c-Src and 
      paxillin was attenuated in a dose-dependent manner. In addition, the paxillin 
      activation entailed p38 MAPK and ERK-responsive signaling, but the JNK activation 
      was less involved. Consistently, oral administration of resveratrol reduced the 
      tissue level of phosphorylated paxillin in the dorsal skin of DNP-HSA-challenged 
      mice. The other tyrosine kinase Tyk2-STAT1 signaling was activated in the dorsal 
      epidermis of antigen-exposed mice, which was associated with allergic 
      inflammation. These results showed that resveratrol inhibited Th2 cytokines- and 
      paxillin-linked allergic responses dependent upon MAPK signaling. Therefore, 
      resveratrol may possess the therapeutic potential of targeting mast cells in 
      preventing the development of allergic inflammation.
FAU - Han, Seon-Young
AU  - Han SY
FAU - Choi, Yean-Jung
AU  - Choi YJ
FAU - Kang, Min-Kyung
AU  - Kang MK
FAU - Park, Jung Han Yoon
AU  - Park JH
FAU - Kang, Young-Hee
AU  - Kang YH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Singapore
TA  - Am J Chin Med
JT  - The American journal of Chinese medicine
JID - 7901431
RN  - 0 (Cytokines)
RN  - 0 (Dinitrophenols)
RN  - 0 (Receptors, IgE)
RN  - 0 (Serum Albumin)
RN  - 0 (Stilbenes)
RN  - 0 (dinitrophenyl-human serum albumin conjugate)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - Q369O8926L (Resveratrol)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Cytokines/*metabolism
MH  - Dinitrophenols/*immunology
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - Hypersensitivity/*drug therapy/*immunology
MH  - Immunoglobulin E/*immunology
MH  - Inflammation/*drug therapy/*immunology
MH  - MAP Kinase Signaling System/drug effects/immunology
MH  - Male
MH  - Mast Cells/*immunology/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Molecular Targeted Therapy
MH  - Phosphorylation/drug effects
MH  - *Phytotherapy
MH  - Receptors, IgE/*immunology
MH  - Resveratrol
MH  - Serum Albumin/*immunology
MH  - Stilbenes/*pharmacology/therapeutic use
MH  - Th2 Cells/immunology
EDAT- 2015/12/02 06:00
MHDA- 2016/09/13 06:00
CRDT- 2015/12/02 06:00
PHST- 2015/12/02 06:00 [entrez]
PHST- 2015/12/02 06:00 [pubmed]
PHST- 2016/09/13 06:00 [medline]
AID - 10.1142/S0192415X15500913 [doi]
PST - ppublish
SO  - Am J Chin Med. 2015;43(8):1605-23. doi: 10.1142/S0192415X15500913.