PMID- 22959927
OWN - NLM
STAT- MEDLINE
DCOM- 20121228
LR  - 20131121
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 264
IP  - 3
DP  - 2012 Nov 1
TI  - Polydatin (PD) inhibits IgE-mediated passive cutaneous anaphylaxis in mice by 
      stabilizing mast cells through modulating Ca(2)(+) mobilization.
PG  - 462-9
LID - S0041-008X(12)00378-X [pii]
LID - 10.1016/j.taap.2012.08.024 [doi]
AB  - Mast cells play a key role in the pathogenesis of asthma and are a promising 
      target for therapeutic intervention in asthma. This study investigated the 
      effects of polydatin (PD), a resveratrol glucoside, on mast cell degranulation 
      upon cross-linking of the high-affinity IgE receptors (FcepsilonRI), as well as the 
      anti-allergic activity of PD in vivo. Herein, we demonstrated that PD treatment 
      for 30 min suppressed FcepsilonRI-mediated mast cell degranulation in a dose-dependent 
      manner. Concomitantly, PD significantly decreased FcepsilonRI-mediated Ca(2)(+) increase in 
      mast cells. The suppressive effects of PD on FcepsilonRI-mediated Ca(2)(+) increase were 
      largely inhibited by using LaCl(3) to block the Ca(2)(+) release-activated Ca(2)(+) 
      channels (CRACs). Furthermore, PD significantly inhibited Ca(2)(+) entry through 
      CRACs evoked by thapsigargin (TG). Knocking down protein expression of Orai1, the 
      pore-forming subunit of CRACs, significantly decreased PD suppression of 
      FcepsilonRI-induced intracellular Ca(2)(+) influx and mast cell degranulation. In a mouse 
      model of mast cell-dependent passive cutaneous anaphylaxis (PCA), in vivo PD 
      administration suppressed mast cell degranulation and inhibited anaphylaxis. 
      Taken together, our data indicate that PD stabilizes mast cells by suppressing 
      FcepsilonRI-induced Ca(2)(+) mobilization mainly through inhibiting Ca(2)(+) entry via CRACs, 
      thus exerting a protective effect against PCA.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Yuan, Meichun
AU  - Yuan M
AD  - Department of Pathophysiology, School of Medicine, Shenzhen University, Shenzhen 
      518060, China.
FAU - Li, Jianjie
AU  - Li J
FAU - Lv, Jingzhang
AU  - Lv J
FAU - Mo, Xucheng
AU  - Mo X
FAU - Yang, Chengbin
AU  - Yang C
FAU - Chen, Xiangdong
AU  - Chen X
FAU - Liu, Zhigang
AU  - Liu Z
FAU - Liu, Jie
AU  - Liu J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120830
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Drugs, Chinese Herbal)
RN  - 0 (FcepsilonRI alpha-chain, human)
RN  - 0 (Glucosides)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptors, IgE)
RN  - 0 (Stilbenes)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - SY7Q814VUP (Calcium)
RN  - XM261C37CQ (polydatin)
SB  - IM
MH  - Animals
MH  - Calcium/*metabolism
MH  - Cell Line
MH  - Drugs, Chinese Herbal/pharmacology
MH  - Female
MH  - Gene Expression Regulation/drug effects
MH  - Glucosides/*pharmacology
MH  - Immunoglobulin E/*physiology
MH  - Mast Cells/*drug effects
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Passive Cutaneous Anaphylaxis/*drug effects
MH  - Reactive Oxygen Species
MH  - Receptors, IgE/genetics/metabolism
MH  - Stilbenes/*pharmacology
EDAT- 2012/09/11 06:00
MHDA- 2012/12/29 06:00
CRDT- 2012/09/11 06:00
PHST- 2012/06/14 00:00 [received]
PHST- 2012/08/22 00:00 [revised]
PHST- 2012/08/23 00:00 [accepted]
PHST- 2012/09/11 06:00 [entrez]
PHST- 2012/09/11 06:00 [pubmed]
PHST- 2012/12/29 06:00 [medline]
AID - S0041-008X(12)00378-X [pii]
AID - 10.1016/j.taap.2012.08.024 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2012 Nov 1;264(3):462-9. doi: 10.1016/j.taap.2012.08.024. 
      Epub 2012 Aug 30.