Inhibitory effects of paeoniflorin on lysophosphatidylcholine-induced inflammatory factor production in human umbilical vein endothelial cells
| Autor: | Jian-Zhe Li, Jian-Hua Wu, Qing-Rui Shao, Xiaomin Dong, Shu-Yi Yu |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
Bridged-Ring Compounds
Cell Survival Anti-Inflammatory Agents Pharmacology Paeonia HMGB1 Benzoates Umbilical vein RAGE (receptor) chemistry.chemical_compound Glucosides Human Umbilical Vein Endothelial Cells Genetics Humans HMGB1 Protein Receptor biology NF-kappa B Lysophosphatidylcholines General Medicine Paeoniflorin Molecular biology Toll-Like Receptor 2 Toll-Like Receptor 4 Lysophosphatidylcholine Gene Expression Regulation chemistry Apoptosis Monoterpenes biology.protein Advanced glycation end-product lipids (amino acids peptides and proteins) |
| Zdroj: | International Journal of Molecular Medicine. 31:493-497 |
| ISSN: | 1791-244X 1107-3756 |
| DOI: | 10.3892/ijmm.2012.1211 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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