作者: Nguyen Dang Hung , Mee Ree Kim , Dai-Eun Sok , None
DOI: 10.1007/S10753-010-9218-Z
关键词:
摘要: Lysophosphatidylcholines (lysoPCs) have been known to be bioactive lipid mediators, which take part in various biological and pathological processes. In the present study, we examined anti-inflammatory actions of 2-docosahexaenoyl lysophosphatidylcholine (2-docosahexaenoyl-lysoPC) vitro as well vivo systems. When RAW 264.7 cells were treated with 2-docoshexaenoyl-lysoPC, a concentration-dependent decrease LPS-induced formation nitric oxide (NO), tumor necrosis factor alpha (TNF-α), or IL-6 was observed. Additionally, oral administration 2-docosahexaenoyl-lysoPC found inhibit zymosan A-induced plasma leakage dose-dependently mice ED50 value 50 μg/kg E max about 65%. Moreover, mechanistic study revealed that action seemed related largely LTC4 inhibition, but not PGE2 inhibition. 2-(17-hydroperoxydocosahexaneoyl)-lysoPC, intravenously administrated, more effective than inhibition leakage, suggesting product from oxygenation by 15-lipoxygenase (LOX), may an active metabolite, intimately responsible for actions, generated 2-docosahexaenoyl-lysoPC. efficient 1-docosahexaenoyl-lysoPC docosahexaenoic acid (DHA) substrate 15-lipoxygenases such soybean LOX-1, leukocyte 12/15-LOX, human 15-LOX-2. Taken altogether, it is suggested its products exert after administration.