Heparin inhibits lipopolysaccharide-induced inflammation via inducing caveolin-1 and activating the p38/mitogen-activated protein kinase pathway in murine peritoneal macrophages

摘要: Abstract Heparin is a soluble glycosaminoglycan largely used as an anti-coagulant drug and with well known anti‑inflammatory effects. However, heparin currently not agent in the clinic due to risk of bleeding its complex mechanism action. The underlying action effector targets have remained be fully elucidated. present study confirmed effects lipopolysaccharide (LPS)‑induced murine peritoneal macrophages through decreasing levels inflammatory cytokines tumor necrosis factor alpha (TNF‑α), interleukin 6 (IL‑6), IL‑8 IL‑1β. Caveolin‑1 participated process it was able induced by heparin. Transfection small interfering RNA caveolin‑1 into attenuated Furthermore, following silencing, p38/mitogen‑activated protein kinase (MAPK) pathway still activated heparin, while extracellular signal‑regulated c‑Jun N‑terminal pathways were inhibited. In conclusion, these results suggested that inhibits LPS‑induced inflammation via inducing activating p38/MAPK macrophages. Revealing mechanisms will aid development for clinical treatment future.