title: Prevention of 1-palmitoyl lysophosphatidylcholine-induced inflammation by polyunsaturated acyl lysophosphatidylcholine.
abstract: OBJECTIVE
  The aim of this study was to examine the inflammation induced by saturated acyl lysophosphatidylcholine (LPC) in vivo and to investigate whether it could be attenuated by the action of polyunsaturated acyl lysophosphatidylcholines (LPCs), which are known as anti-inflammatory lipid mediators.
  
  
  METHODS
  First, saturated acyl LPC was administered intraperitoneally (i.p.) to mice and the inflammatory profile was extensively characterized. Subsequently, the preventive effect of polyunsaturated acyl LPCs, i.p. administered 30 min after saturated acyl LPC, was evaluated by measuring indices of inflammation such as leukocyte migration, plasma leakage, and eicosanoid or cytokine formation by light microscopy, Evans blue dye as indicator, and enzyme-linked immunosorbent assay, respectively.
  
  
  RESULTS
  Saturated acyl LPCs as LPC16:0 (100 mg/kg, i.p.) proved to be an effective inflammation inducer which causes a significant increase in plasma leakage, leukocyte migration into peritoneum and elevation of pro-inflammatory mediators. Interestingly, LPC20:4 and LPC22:6 (50 and 150 μg/kg) significantly nullified LPC16:0-induced inflammation. The anti-inflammatory effects of LPC20:4 and LPC22:6 were related to down-regulation of leukocyte extravasation, plasma leakage, and formation of pro-inflammatory mediators (IL-5, IL-6, NO, 12-HETE and PGE(2)) stimulated by LPC16:0, and up-regulation of anti-inflammatory mediators (IL-4 and IL-10).
  
  
  CONCLUSIONS
  These results indicated that the pro-inflammatory activity of saturated acyl LPCs could be antagonized by the actions of polyunsaturated acyl LPCs, anti-inflammatory lipid mediators.
authors.affiliation: College of Pharmacy, Chungnam National University, Yuseong-Gu, Gungdong, Daejeon, Korea. hung_hanoi_vietnam@yahoo.com
authors.forename: Nguyen Dang
authors.initials: ND
authors.lastname: Hung
authors.forename: Dai-Eun
authors.initials: DE
authors.lastname: Sok
authors.forename: Mee Ree
authors.initials: MR
authors.lastname: Kim
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002199:Capillary Permeability / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D007249:Inflammation / Q000139:chemically induced*; D018836:Inflammation Mediators / Q000378:metabolism; D007962:Leukocytes / Q000187:drug effects / Q000502:physiology; D008244:Lysophosphatidylcholines / Q000494:pharmacology* / Q000633:toxicity; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR
chemical_list: C470482:1-hydroxy-2-hexadecanoyl-sn-glycero-3-phosphocholine; D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D008244:Lysophosphatidylcholines; C006065:We 201