PMID- 32135490
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240227
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 82
DP  - 2020 Mar 2
TI  - Attenuation of pristimerin on TNF-alpha-induced endothelial inflammation.
PG  - 106326
LID - S1567-5769(19)32706-7 [pii]
LID - 10.1016/j.intimp.2020.106326 [doi]
AB  - OBJECTIVE: Pristimerin is known to have anti-cancer and anti-inflammatory 
      activities; however, its therapeutic mechanism has not been described. In this 
      study, to investigate the therapeutic mechanism of pristimerin, we examined the 
      effect of pristimerin on TNF-alpha-induced endothelial inflammatory response both in 
      vitro and in vivo. METHODS: Leukocyte-endothelium Adhesion Assay was use to 
      evaluate the endothelial cell-monocyte interaction. Western blotting was used to 
      confirm protein expression. NF-kappaB p65 nuclear translocation in endothelial cells 
      was detected using immunofluorescent microscopy. In vivo leukocyte infiltration 
      was evaluated using acute lung inflammation model. RESULTS: Pristimerin 
      profoundly inhibited TNF-alpha-induced adhesion of monocytes to human endothelial 
      cells and the leukocyte transmigration. Pristimerin dramatically inhibited the 
      expression of TNF-alpha-induced endothelial adhesion molecules (intercellular 
      adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)) and 
      the pro-inflammatory cytokine (IL-6, IL-8 and monocyte chemoattractant protein-1 
      (MCP-1)). Pristimerin suppressed the penetration of the leukocyte in the acute 
      lung injury mice model. Furthermore, pristimerin also suppressed the 
      TNF-alpha-activated Nuclear factor kappa B (NF-kappaB) activation. CONCLUSIONS: 
      Pristimerin has the anti-inflammatory properties in endothelial cells, at least 
      in part, through the suppression of NF-kappaB activation, which may have a potential 
      therapeutic effects for inflammatory vascular diseases.
CI  - Copyright (c) 2020. Published by Elsevier B.V.
FAU - Liang, Jiang
AU  - Liang J
AD  - Collaborative Innovation Center of Miao Medicine, Guizhou University of 
      Traditional Chinese Medicine, Guiyang, Guizhou, China; Department of Rheamatology 
      and Hematology, The First Affiliated Hospital, Guizhou University of Traditional 
      Chinese Medicine, Guiyang, Guizhou, China.
FAU - Yuan, Shiwen
AU  - Yuan S
AD  - Department of Rheumatology, Guangzhou First People's Hospital, School of 
      Medicine, South China University of Technology, Guangzhou, Guangdong, China.
FAU - Wang, Xiaohua
AU  - Wang X
AD  - Department of Nephrology,Kidney and Urology Center, The Seventh Affiliated 
      Hospital of Sun Yat-Sen University, ShenZhen, Guandong, China.
FAU - Lei, Yan
AU  - Lei Y
AD  - Department of Nephrology,Kidney and Urology Center, The Seventh Affiliated 
      Hospital of Sun Yat-Sen University, ShenZhen, Guandong, China.
FAU - Zhang, Xuemei
AU  - Zhang X
AD  - Department of Nephrology,Kidney and Urology Center, The Seventh Affiliated 
      Hospital of Sun Yat-Sen University, ShenZhen, Guandong, China.
FAU - Huang, Mingcheng
AU  - Huang M
AD  - Department of Nephrology,Kidney and Urology Center, The Seventh Affiliated 
      Hospital of Sun Yat-Sen University, ShenZhen, Guandong, China. Electronic 
      address: ouyh3@mail2.sysu.edu.cn.
FAU - Ouyang, Hui
AU  - Ouyang H
AD  - Department of Digestive Medicine Center, The Seventh Affiliated Hospital, Sun 
      Yat-Sen University, ShenZhen, Guandong, China. Electronic address: 
      huangcongen2018@sina.com.
LA  - eng
PT  - Journal Article
DEP - 20200302
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
SB  - IM
OTO - NOTNLM
OT  - Endothelial cells
OT  - Pristimerin
OT  - Vascular inflammation
COIS- Declaration of Competing Interest The authors declared that there is no conflict 
      of interest.
EDAT- 2020/03/07 06:00
MHDA- 2020/03/07 06:01
CRDT- 2020/03/06 06:00
PHST- 2019/11/23 00:00 [received]
PHST- 2020/01/30 00:00 [revised]
PHST- 2020/02/14 00:00 [accepted]
PHST- 2020/03/07 06:01 [medline]
PHST- 2020/03/07 06:00 [pubmed]
PHST- 2020/03/06 06:00 [entrez]
AID - S1567-5769(19)32706-7 [pii]
AID - 10.1016/j.intimp.2020.106326 [doi]
PST - aheadofprint
SO  - Int Immunopharmacol. 2020 Mar 2;82:106326. doi: 10.1016/j.intimp.2020.106326.