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

Li,Jian-Zhe; Wu,Jian-Hua; Yu,Shu-Yi; Shao,Qing-Rui; Dong,Xiao-Min

doi:10.3892/ijmm.2012.1211

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

Authors:
- Jian-Zhe Li
- Jian-Hua Wu
- Shu-Yi Yu
- Qing-Rui Shao
- Xiao-Min Dong
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Affiliations: Department of Pharmacy, Ruikang Hospital, Guangxi University of Traditional Chinese Medicine, Nanning, Guangxi 530011, P.R. China, Department of Pharmacy, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China, Modern Analysis and Testing Center, Central South University, Changsha, Hunan 410078, P.R. China
Published online on: December 13, 2012 https://doi.org/10.3892/ijmm.2012.1211
Pages: 493-497

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Abstract

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 µmol/l) 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-κB (NF-κB) 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-κB pathway.

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