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本实验从花生四烯酸(AA)代谢途径探讨麝香抗炎作用机理,用14_C标记花生四烯酸(14_C-AA)标记白细胞,观察麝香对大鼠角叉菜胶炎性渗出液中白细胞内AA释放及其代谢酶产物——白三烯B_4(LTB_4)和5-羟基廿碳四烯酸(5-HETE)生成的影响。实验表明,麝香水提物(MWF)浓度为6.25～37.5μg/ml时,抑制AA释放,释放量比对照组减少50～70％,但不抑制LTB_4和5-HETE的生成;MWF浓度加大至80μg/ml时,AA释放增加至对照组的1.5倍,但LTB_4和5-HETE生物合成却分别抑制了66.7％和90％。提示MWF具有抑制磷脂酶A_2(PLA_2)活性的作用,大剂量时又进一步阻断了AA代谢酶,如5-脂氧酶(5-LO),从而抑制了AA的过氧化,减少炎症介质,如LTB_4、5-HETE等的生成。
In this study, the mechanism of anti-inflammatory effect of musk was studied from arachidonic acid (AA) metabolism pathway. The leukotrienes were labeled with 14_C-labeled arachidonic acid (14_C-AA) to observe the effects of musk on leukocyte Release of AA and the production of 5-HETE, the metabolites of leukotriene B_4 (LTB_4). The results showed that the MWF concentration of 6.25 ~ 37.5μg / ml inhibited the release of AA, which was 50 ~ 70% less than that of the control group, but did not inhibit the formation of LTB_4 and 5-HETE. The MWF concentration was increased At 80μg / ml, AA release increased to 1.5 times that of the control group, but biosynthesis of LTB_4 and 5-HETE inhibited 66.7% and 90%, respectively. These results suggest that MWF can inhibit the activity of PLA2 and further block the metabolism of AA metabolites such as 5-LO (5-LO) at high doses, thereby inhibiting the peroxidation of AA and reducing the inflammatory mediators. Such as the LTB_4,5-HETE generation.