Suppressive effects of pelargonidin on lipopolysaccharide-induced inflammatory responses

被引:17
|
作者
Lee, Bong-Seon [1 ]
Lee, Changhun [1 ]
Yang, Sumin [1 ]
Park, Eui Kyun [2 ]
Ku, Sae-Kwang [3 ]
Bae, Jong-Sup [1 ]
机构
[1] Kyungpook Natl Univ, Res Inst Pharmaceut Sci, Coll Pharm, CMRI,Plus KNU Multiom Based Creat Drug Res Team B, Daegu 41566, South Korea
[2] Kyungpook Natl Univ, Sch Dent, Dept Pathol & Regenerat Med, Daegu 41940, South Korea
[3] Daegu Haany Univ, Dept Anat & Histol, Coll Korean Med, Gyongsan 38610, South Korea
基金
新加坡国家研究基金会;
关键词
Pelargonidin; Lipopolysaccharide; Inflammation; Barrier integrity; NF-KAPPA-B; ACTIVATED PROTEIN-KINASE; ENDOTHELIAL BARRIER DYSFUNCTION; CELL-ADHESION MOLECULES; TNF-ALPHA; GENE-EXPRESSION; LUNG INJURY; MECHANISMS; INDUCTION; LEUKOCYTE;
D O I
10.1016/j.cbi.2019.02.007
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pelargonidin (PEL) is a well-known red pigment found in plants, and has been reported as having important biological activities that are potentially beneficial for human health. Here, we tested the possible use of PEL in the treatment of lipopolysaccharide (LPS)-mediated vascular inflammatory responses. The anti-inflammatory activities of PEL were determined by measuring permeability, neutrophils adhesion and migration, and activation of pro-inflammatory proteins in LPS-activated human umbilical vein endothelial cells (HUVECs) and mice. We found that PEL inhibited LPS-induced barrier disruption, expression of cell adhesion molecules (CAMs), and adhesion/transendothelial migration of neutrophils to human endothelial cells. PEL also suppressed LPS-induced hyperpermeability and leukocytes migration in vivo. Furthermore, PEL suppressed the production of tumor necrosis factor-alpha (TNF-alpha) or Interleukin (IL)-6 and the activation of nuclear factor-kappa B (NF-kappa B) or extracellular regulated kinases (ERK) 1/2 by LPS. Moreover, treatment with PEL resulted in reduced LPS-induced lethal endotoxemia. These results suggest that PEL possesses anti-inflammatory functions by inhibiting hyperpermeability, expression of CAMs, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases.
引用
收藏
页码:67 / 73
页数:7
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