PMID- 27643663
OWN - NLM
STAT- MEDLINE
DCOM- 20170515
LR  - 20171116
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 40
DP  - 2016 Nov
TI  - Therapeutic potential of Oroxylin A in rheumatoid arthritis.
PG  - 294-299
LID - S1567-5769(16)30380-0 [pii]
LID - 10.1016/j.intimp.2016.09.006 [doi]
AB  - Excessive inflammation contributes greatly to the pathogenesis and development of 
      rheumatoid arthritis (RA). Oroxylin A (OA) is a natural anti-inflammatory 
      flavonoid compound. In this study, we investigated the effects of OA on 
      collagen-induced arthritis (CIA) and human RA fibroblast-like synoviocytes (FLS). 
      CIA was induced in DBA/1 mice and mice were intraperitoneally treated with OA 
      (10mg/kg) for 10days. Arthritis severity was evaluated every day and the 
      histopathologic examination of joints was done. Serum levels of anti-collagen II 
      antibodies (anti-CII Abs) and cytokines were determined by ELISA. Frequency of 
      regulatory T cells (Tregs) and Th17 cells in draining inguinal lymph nodes (ILN) 
      was quantified by flow cytometry. FLS from patients with active RA were treated 
      with varying doses of oroxylin A, followed by stimulation with tumor necrosis 
      factor (TNF)-alpha (10ng/mL). The production of cytokines was measured by ELISA. 
      Signal transduction proteins were examined by western blot. OA significantly 
      diminished the arthritis and histological damage. Serum anti-CII Abs, IL-1beta, 
      IL-6, TNFalpha, and IL-17 were significantly diminished by OA treatment. Analysis of 
      CD4+T cell populations in OA-treated mice showed an increase in Tregs and 
      reduction in Th17 cells in the ILN. In vitro, OA decreased the secretion of IL-1beta 
      and IL-6 from TNFalpha-stimulated RA FLS in a dose-dependent manner. TNFalpha-induced p38 
      MAPK, ERK1/2 and NF-kappaB signaling pathways were suppressed by OA. Our results 
      indicate that OA exerts an anti-inflammatory activity and may have therapeutic 
      potential for human RA.
CI  - Copyright (c) 2016 Elsevier B.V. All rights reserved.
FAU - Wang, Yu-Ling
AU  - Wang YL
AD  - Department of Rheumatology and Immunology, Linyi People's Hospital, Linyi 276003, 
      Shandong, China.
FAU - Gao, Ju-Mei
AU  - Gao JM
AD  - Department of Rheumatology and Immunology, Yishui Central Hospital, Linyi 276400, 
      Shandong, China.
FAU - Xing, Li-Zhi
AU  - Xing LZ
AD  - Department of Endocrinology, Linyi People's Hospital, Linyi 276003, Shandong, 
      China. Electronic address: xing_lizhi@yeah.net.
LA  - eng
PT  - Journal Article
DEP - 20160916
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (Flavonoids)
RN  - 53K24Z586G (5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one)
SB  - IM
MH  - Animals
MH  - Ankle Joint/drug effects/pathology
MH  - Anti-Inflammatory Agents/pharmacology/*therapeutic use
MH  - Arthritis, Experimental/*drug therapy/immunology/pathology
MH  - Arthritis, Rheumatoid/*drug therapy/immunology/pathology
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Cytokines/immunology
MH  - Flavonoids/pharmacology/*therapeutic use
MH  - Humans
MH  - Lymph Nodes/cytology/immunology
MH  - Male
MH  - Mice, Inbred DBA
MH  - Synoviocytes/drug effects/immunology
MH  - T-Lymphocytes, Regulatory/immunology
MH  - Th17 Cells/immunology
OTO - NOTNLM
OT  - Collagen-induced arthritis
OT  - Fibroblast-like synoviocytes
OT  - Oroxylin A
OT  - Rheumatoid arthritis
EDAT- 2016/09/20 06:00
MHDA- 2017/05/16 06:00
CRDT- 2016/09/20 06:00
PHST- 2016/06/24 00:00 [received]
PHST- 2016/08/26 00:00 [revised]
PHST- 2016/09/06 00:00 [accepted]
PHST- 2016/09/20 06:00 [pubmed]
PHST- 2017/05/16 06:00 [medline]
PHST- 2016/09/20 06:00 [entrez]
AID - S1567-5769(16)30380-0 [pii]
AID - 10.1016/j.intimp.2016.09.006 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2016 Nov;40:294-299. doi: 10.1016/j.intimp.2016.09.006. Epub 
      2016 Sep 16.