PMID- 23494816
OWN - NLM
STAT- MEDLINE
DCOM- 20140328
LR  - 20211021
IS  - 1861-0293 (Electronic)
IS  - 1340-3443 (Linking)
VI  - 67
IP  - 4
DP  - 2013 Oct
TI  - Acteoside inhibits type Iota allergy through the down-regulation of Ca/NFAT and JNK 
      MAPK signaling pathways in basophilic cells.
PG  - 790-8
LID - 10.1007/s11418-013-0753-4 [doi]
AB  - We have previously reported that acteoside inhibits the release of 
      beta-hexosaminidase from immunoglobulin E (IgE)-sensitized and bovine serum 
      albumin-stimulated rat basophilic leukemia cells as well as the intracellular 
      calcium level, release of histamine from, and production of tumor necrosis 
      factor-alpha and interleukin-4 in human basophilic (KU812) cells. However, the 
      molecular mechanism underlying the anti-allergic effects of acteoside has not yet 
      been elucidated. Here, we used microarray analysis to determine the global gene 
      expression profile of KU812 cells treated with acteoside and calcium ionophore 
      A23187 plus phorbol-12-myristate 13-acetate (A23187+PMA), and the results were 
      validated by real-time polymerase chain reaction (PCR) and Western blotting. 
      Microarray analysis results showed that of the 201 genes in the microarray, 149 
      genes were up-regulated, while 52 genes were down-regulated. The significantly 
      down-regulated genes have functions as chemokine and IgE receptors, as well as 
      for immune response. Results of the validation of the microarray results using 
      real-time PCR showed a significant decrease in the expressions of Fc fragment of 
      IgE, high affinity I, receptor for; alpha polypeptide (FCER1A) and nuclear factor 
      of activated T cell, cytoplasmic, calcineurin-dependent 1 (NFATC1) genes. 
      Furthermore, Western blotting showed a decrease in the phosphorylation of 
      mitogen-activated protein kinase (MAPK) Jun N terminal kinase (JNK), revealing 
      the role of JNK MAPK in acteoside-mediated allergy inhibition. We determined that 
      the anti-allergy effects of acteoside were due to the down-regulation of the 
      expressions of the chemokine ligand 1 (CCL1), CCL2, CCL3, CCL4, FCER1A and NFATC1 
      genes and the inhibition of the MAPK pathway through decreased JNK 
      phosphorylation.
FAU - Motojima, Hideko
AU  - Motojima H
AD  - Alliance for Research on North Africa (ARENA), University of Tsukuba, Tennodai 
      1-1-1, Tsukuba, Ibaraki, 305-8572, Japan.
FAU - Villareal, Myra O
AU  - Villareal MO
FAU - Iijima, Rieko
AU  - Iijima R
FAU - Han, Junkyu
AU  - Han J
FAU - Isoda, Hiroko
AU  - Isoda H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130315
PL  - Japan
TA  - J Nat Med
JT  - Journal of natural medicines
JID - 101518405
RN  - 0 (Anti-Allergic Agents)
RN  - 0 (Calcium Ionophores)
RN  - 0 (Glucosides)
RN  - 0 (NFATC Transcription Factors)
RN  - 0 (Phenols)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, IgE)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37H9VM9WZL (Calcimycin)
RN  - 3TGX09BD5B (acteoside)
RN  - 56937-68-9 (phorbolol myristate acetate)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Animals
MH  - Anti-Allergic Agents/chemistry/*pharmacology
MH  - Basophils/*drug effects/immunology
MH  - Calcimycin/pharmacology
MH  - Calcium Ionophores/pharmacology
MH  - Cell Line
MH  - Cistanche/chemistry
MH  - Down-Regulation/drug effects
MH  - Glucosides/chemistry/*pharmacology
MH  - Humans
MH  - Hypersensitivity, Immediate/immunology
MH  - Interleukin-4/metabolism
MH  - JNK Mitogen-Activated Protein Kinases/*metabolism
MH  - MAP Kinase Signaling System/drug effects
MH  - NFATC Transcription Factors/genetics/metabolism
MH  - Phenols/chemistry/*pharmacology
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Receptors, IgE/genetics/metabolism
MH  - Signal Transduction/*drug effects
MH  - Tetradecanoylphorbol Acetate/analogs & derivatives/pharmacology
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2013/03/16 06:00
MHDA- 2014/03/29 06:00
CRDT- 2013/03/16 06:00
PHST- 2012/10/10 00:00 [received]
PHST- 2013/01/31 00:00 [accepted]
PHST- 2013/03/16 06:00 [entrez]
PHST- 2013/03/16 06:00 [pubmed]
PHST- 2014/03/29 06:00 [medline]
AID - 10.1007/s11418-013-0753-4 [doi]
PST - ppublish
SO  - J Nat Med. 2013 Oct;67(4):790-8. doi: 10.1007/s11418-013-0753-4. Epub 2013 Mar 
      15.