Inhibitory effects of paeoniflorin on lysophosphatidylcholine-induced inflammatory factor production in human umbilical vein endothelial cells

被引:42
作者
Li, Jian-Zhe [1 ]
Wu, Jian-Hua [2 ]
Yu, Shu-Yi [3 ]
Shao, Qing-Rui [1 ]
Dong, Xiao-Min [2 ]
机构
[1] Guangxi Univ Tradit Chinese Med, Dept Pharm, Ruikang Hosp, Nanning 530011, Guangxi, Peoples R China
[2] Wuhan Univ, Zhongnan Hosp, Dept Pharm, Wuhan 430071, Hubei, Peoples R China
[3] Cent S Univ, Modern Anal & Testing Ctr, Changsha 410078, Hunan, Peoples R China
关键词
paeoniflorin; lysophosphatidylcholine; inflammatory factors; high mobility group box-1; human umbilical vein endothelial cells; FACTOR-KAPPA-B; PAEONIA-LACTIFLORA; HMGB1; EXPRESSION; ACTIVATION; PROTECTS; RESPONSES; BARRIER; INJURY; ALPHA;
D O I
10.3892/ijmm.2012.1211
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Lysophosphatidylcholine (LPC) plays an important role in atherosclerosis through initiation of endothelial inflammation response. Paeoniflorin (PEF), isolated from the dry root of Paeonia, has been reported to exert an anti-inflammatory effect, but the exact mechanism is not fully understood. The aim of this study was to investigate the inhibitory effects of PEF on LPC-induced inflammatory factor production and the underlying mechanisms. In human umbilical vein endothelial cells (HUVECs), different concentrations (1, 10 or 100 mu mol/1) of PEF were added 2 h prior to exposure to LPC (10 mg/l) for 24 h. The results showed that PEF significantly inhibited LPC-induced inflammatory factor production. In addition, PEF was also able to suppress the enhanced high mobility group box-1 (HMGB1) expression and release, upregulated expression of receptor for advanced glycation end product (RAGE), Toll-like receptor (TLR)-2 and TLR-4, and increased nuclear factor-kappa B (NF-kappa B) activity induced by LPC. Our results suggest that PEF suppresses LPC-induced inflammatory factor production through inhibition of the HMGB1-RAGE/TLR-2/TLR-4-NF-kappa B pathway.
引用
收藏
页码:493 / 497
页数:5
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