PMID- 32179246
OWN - NLM
STAT- MEDLINE
DCOM- 20210308
LR  - 20210308
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 83
DP  - 2020 Jun
TI  - Alogliptin inhibits IL-1beta-induced inflammatory response in fibroblast-like 
      synoviocytes.
PG  - 106372
LID - S1567-5769(19)32874-7 [pii]
LID - 10.1016/j.intimp.2020.106372 [doi]
AB  - Excessive production of pro-inflammatory cytokines such as interleukin (IL)-1beta 
      plays an important role in the chronic inflammation in fibroblast-like 
      synoviocytes (FLS) in rheumatoid arthritis (RA). Alogliptin, an important 
      selective dipeptidyl peptidase-4 (DPP-4) inhibitor licensed for the treatment of 
      type 2 diabetes, has displayed a wide range of pharmacological capacities. In the 
      present study, we aimed to investigate whether alogliptin possessed a protective 
      effect against IL-1beta-induced insult in FLS. Our results indicate that alogliptin 
      treatment ameliorated IL-1beta-induced production of reactive oxygen species, the 
      expression of matrix metalloproteinase-3 (MMP-3) and MMP-13, secretions of tumor 
      necrosis factor-alpha (TNF-alpha), IL-6, and IL-8. Additionally, we found that alogliptin 
      inhibited c-Jun N-terminal kinase (JNK)/activator protein 1 (AP-1) signaling by 
      reducing IL-1beta-induced phosphorylation of JNK, the expression of c-Jun and c-Fos, 
      and the luciferase activity of AP-1. Importantly, alogliptin suppressed 
      IL-1beta-induced activation of IkappaBalpha/NF-kappaB signaling by preventing the 
      phosphorylation and degradation of IkappaBalpha, nuclear translocation of NF-kappaB p65, as 
      well as the luciferase activity of AP-1. These findings suggest that alogliptin 
      might have therapeutic potential for the treatment of chronic inflammation in RA.
CI  - Copyright (c) 2020 Elsevier B.V. All rights reserved.
FAU - Guo, Qi
AU  - Guo Q
AD  - Department of Orthopedic, First People's Hospital of Shangqiu, Shangqiu, Henan 
      476000, China. Electronic address: guoqi356@163.com.
FAU - Zhang, Shun
AU  - Zhang S
AD  - Department of Orthopedic, First People's Hospital of Shangqiu, Shangqiu, Henan 
      476000, China.
FAU - Huang, Jiuqin
AU  - Huang J
AD  - Department of Orthopedic, First People's Hospital of Shangqiu, Shangqiu, Henan 
      476000, China.
FAU - Liu, Ke
AU  - Liu K
AD  - Department of Orthopedic, Henan Provincial People's Hospital, Zhengzhou, Henan 
      450003, China.
LA  - eng
PT  - Journal Article
DEP - 20200314
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Dipeptidyl-Peptidase IV Inhibitors)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1beta)
RN  - 0 (NF-kappa B)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Transcription Factor AP-1)
RN  - EC 3.4.24.- (Matrix Metalloproteinase 13)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
SB  - IM
MH  - Arthritis, Rheumatoid/*metabolism
MH  - Cells, Cultured
MH  - Dipeptidyl-Peptidase IV Inhibitors/*therapeutic use
MH  - Fibroblasts/*physiology
MH  - Humans
MH  - Inflammation/*metabolism
MH  - Inflammation Mediators/metabolism
MH  - Interleukin-1beta/*metabolism
MH  - Matrix Metalloproteinase 13/metabolism
MH  - Matrix Metalloproteinase 3/metabolism
MH  - NF-kappa B/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction
MH  - Synoviocytes/*drug effects/physiology
MH  - Transcription Factor AP-1/metabolism
OTO - NOTNLM
OT  - Fibroblast-like synoviocytes (FLS)
OT  - IL-1beta
OT  - Inflammation
OT  - NF-kappaB
OT  - Oxidative stress
OT  - Rheumatoid arthritis (RA)
EDAT- 2020/03/18 06:00
MHDA- 2021/03/09 06:00
CRDT- 2020/03/18 06:00
PHST- 2019/12/08 00:00 [received]
PHST- 2020/02/24 00:00 [revised]
PHST- 2020/03/02 00:00 [accepted]
PHST- 2020/03/18 06:00 [pubmed]
PHST- 2021/03/09 06:00 [medline]
PHST- 2020/03/18 06:00 [entrez]
AID - S1567-5769(19)32874-7 [pii]
AID - 10.1016/j.intimp.2020.106372 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2020 Jun;83:106372. doi: 10.1016/j.intimp.2020.106372. Epub 
      2020 Mar 14.