PMID- 35784390
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220716
IS  - 1976-8354 (Print)
IS  - 2151-2485 (Electronic)
IS  - 1976-8354 (Linking)
VI  - 26
IP  - 3
DP  - 2022
TI  - Cynarin attenuates LPS-induced endothelial inflammation via upregulation of the 
      negative regulator MKP-3.
PG  - 119-128
LID - 10.1080/19768354.2022.2077438 [doi]
AB  - Clinical observations have revealed that non-resolving low-grade inflammation is 
      linked to the pathogenesis of chronic inflammatory diseases, for example 
      arthritis, atherosclerosis, Alzheimer's disease, diabetes, and chronic kidney 
      disease. Interestingly, low levels of circulating lipopolysaccharides (LPS) 
      derived from the outer membrane of gram-negative bacteria appear to be one of the 
      primary causes of persistent low-grade inflammation. The inner surface of the 
      blood vessels is lined with endothelial cells; therefore, even low levels of 
      circulating LPS can directly activate these cells and elicit specific cellular 
      responses, such as an increase in the expression levels of cell adhesion 
      molecules and proinflammatory mediators. In endothelial cells, LPS exposure 
      results in an inflammatory response through activation of nuclear factor-kappa B 
      (NF-kappaB) and mitogen-activated protein kinases. Cynarin, a phytochemical found in 
      artichokes, has several pharmacological properties against endothelial 
      inflammation. In the present study, we discovered that cynarin suppressed the 
      LPS-induced increase in the expression levels of vascular cell adhesion 
      molecule-1 and proinflammatory mediators such as monocyte chemoattractant 
      protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta in 
      EA.hy926 cells. Further, cynarin inhibited the activation of p38 and NF-kappaB 
      pathways by inducing the negative regulator mitogen-activated protein kinase 
      phosphatase 3 (MKP-3) in LPS-stimulated EA.hy926 cells. In conclusion, cynarin 
      alleviates inflammation by upregulating MKP-3, a negative regulator of p38 and 
      NF-kappaB, and it may be a therapeutic option for treating endothelial 
      inflammation-related diseases.
CI  - (c) 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & 
      Francis Group.
FAU - Kim, Da Bin
AU  - Kim DB
AD  - Department of Molecular Medicine, College of Medicine, Inha University, Incheon, 
      Republic of Korea.
AD  - Program in Biomedical Science and Engineering, College of Medicine, Inha 
      University, Incheon, Republic of Korea.
FAU - Unenkhuu, Banzragchgarav
AU  - Unenkhuu B
AD  - Department of Molecular Medicine, College of Medicine, Inha University, Incheon, 
      Republic of Korea.
FAU - Kim, Grace Jisoo
AU  - Kim GJ
AD  - Yongsan International School of Seoul, Seoul, Republic of Korea.
FAU - Kim, Seung-Woo
AU  - Kim SW
AD  - Department of Biomedical Sciences, College of Medicine, Inha University, Incheon, 
      Republic of Korea.
FAU - Kim, Hong Seok
AU  - Kim HS
AD  - Department of Molecular Medicine, College of Medicine, Inha University, Incheon, 
      Republic of Korea.
LA  - eng
PT  - Journal Article
DEP - 20220520
PL  - England
TA  - Anim Cells Syst (Seoul)
JT  - Animal cells and systems
JID - 101478641
PMC - PMC9246029
OTO - NOTNLM
OT  - Cynarin
OT  - MKP-3
OT  - endothelial inflammation
OT  - endotoxin
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/07/06 06:00
MHDA- 2022/07/06 06:01
PMCR- 2022/05/20
CRDT- 2022/07/05 10:24
PHST- 2022/07/05 10:24 [entrez]
PHST- 2022/07/06 06:00 [pubmed]
PHST- 2022/07/06 06:01 [medline]
PHST- 2022/05/20 00:00 [pmc-release]
AID - 2077438 [pii]
AID - 10.1080/19768354.2022.2077438 [doi]
PST - epublish
SO  - Anim Cells Syst (Seoul). 2022 May 20;26(3):119-128. doi: 
      10.1080/19768354.2022.2077438. eCollection 2022.