PMID- 23472193
OWN - NLM
STAT- MEDLINE
DCOM- 20131203
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 3
DP  - 2013
TI  - Acetylcorynoline impairs the maturation of mouse bone marrow-derived dendritic 
      cells via suppression of IkappaB kinase and mitogen-activated protein kinase 
      activities.
PG  - e58398
LID - 10.1371/journal.pone.0058398 [doi]
LID - e58398
AB  - BACKGROUND: Dendritic cells (DCs) are major modulators in the immune system. One 
      active field of research is the manipulation of DCs as pharmacological targets to 
      screen novel biological modifiers for the treatment of inflammatory and 
      autoimmune disorders. Acetylcorynoline is the major alkaloid component derived 
      from Corydalis bungeana herbs. We assessed the capability of acetylcorynoline to 
      regulate lipopolysaccharide (LPS)-stimulated activation of mouse bone 
      marrow-derived DCs. METHODOLOGY/PRINCIPAL FINDINGS: Our experimental data showed 
      that treatment with up to 20 microM acetylcorynoline does not cause cytotoxicity in 
      cells. Acetylcorynoline significantly inhibited the secretion of tumor necrosis 
      factor-alpha, interleukin-6, and interleukin-12p70 by LPS-stimulated DCs. The 
      expression of LPS-induced major histocompatibility complex class II, CD40, and 
      CD86 on DCs was also decreased by acetylcorynoline, and the endocytic capacity of 
      LPS-stimulated DCs was restored by acetylcorynoline. In addition, LPS-stimulated 
      DC-elicited allogeneic T-cell proliferation was blocked by acetylcorynoline, and 
      the migratory ability of LPS-stimulated DCs was reduced by acetylcorynoline. 
      Moreover, acetylcorynoline significantly inhibits LPS-induced activation of IkappaB 
      kinase and mitogen-activated protein kinase. Importantly, administration of 
      acetylcorynoline significantly attenuates 2,4-dinitro-1-fluorobenzene-induced 
      delayed-type hypersensitivity. CONCLUSIONS/SIGNIFICANCE: Acetylcorynoline may be 
      one of the potent immunosuppressive agents through the blockage of DC maturation 
      and function.
FAU - Fu, Ru-Huei
AU  - Fu RH
AD  - Graduate Institute of Immunology, China Medical University, and Center for 
      Neuropsychiatry, China Medical University Hospital, Taichung, Taiwan. 
      rhfu@mail.cmu.edu.tw
FAU - Wang, Yu-Chi
AU  - Wang YC
FAU - Liu, Shih-Ping
AU  - Liu SP
FAU - Chu, Ching-Liang
AU  - Chu CL
FAU - Tsai, Rong-Tzong
AU  - Tsai RT
FAU - Ho, Yu-Chen
AU  - Ho YC
FAU - Chang, Wen-Lin
AU  - Chang WL
FAU - Chiu, Shao-Chih
AU  - Chiu SC
FAU - Harn, Horng-Jyh
AU  - Harn HJ
FAU - Shyu, Woei-Cherng
AU  - Shyu WC
FAU - Lin, Shinn-Zong
AU  - Lin SZ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130305
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Berberine Alkaloids)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Plant Extracts)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (acetylcorynoline)
RN  - 187348-17-0 (Interleukin-12)
RN  - EC 2.7.11.10 (I-kappa B Kinase)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Berberine Alkaloids/*pharmacology
MH  - Bone Marrow Cells/*cytology/drug effects
MH  - Cell Membrane/metabolism
MH  - Cell Movement
MH  - Cell Survival
MH  - Corydalis/metabolism
MH  - Dendritic Cells/*cytology/drug effects/metabolism
MH  - Endocytosis
MH  - I-kappa B Kinase/*metabolism
MH  - Inflammation
MH  - Interleukin-12/metabolism
MH  - Interleukin-6/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Mice
MH  - Mitogen-Activated Protein Kinases/*metabolism
MH  - Plant Extracts/pharmacology
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC3589392
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/03/09 06:00
MHDA- 2013/12/16 06:00
PMCR- 2013/03/05
CRDT- 2013/03/09 06:00
PHST- 2012/11/05 00:00 [received]
PHST- 2013/02/04 00:00 [accepted]
PHST- 2013/03/09 06:00 [entrez]
PHST- 2013/03/09 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
PHST- 2013/03/05 00:00 [pmc-release]
AID - PONE-D-12-34112 [pii]
AID - 10.1371/journal.pone.0058398 [doi]
PST - ppublish
SO  - PLoS One. 2013;8(3):e58398. doi: 10.1371/journal.pone.0058398. Epub 2013 Mar 5.