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目的:观察新型非甾体抗炎药2-(2,4-二氯苯基)-3-(3,5-二甲氧基苯基)-苯丙烯酰胺(AL-017)对诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)及环氧化酶2(cyclooxygenase-2,COX-2)的抑制作用,探讨其分子机制。方法:体外培养小鼠巨噬细胞(RAW264.7),用脂多糖(LPS)刺激,观察AL-017对一氧化氮(nitrogen monoxidum,NO)释放、iNOS总酶活、iNOS及COX-2的mRNA表达水平、p38信号通路有无影响。结果:AL-017可以显著抑制LPS引起的NO的释放,使LPS刺激下增高的iNOS酶活性降低,同时显著下调LPS诱导的iNOS及COX-2 mRNA表达水平的升高,并可明显抑制LPS刺激下p38丝裂原活化蛋白激酶(p38MAPK)的磷酸化。结论:AL-017可有效抑制LPS引起的小鼠巨噬细胞炎症反应,其抗炎机制可能与抑制p38MAPK磷酸化有关。
OBJECTIVE: To observe the effect of a novel non-steroidal anti-inflammatory drug 2- (2,4-dichlorophenyl) -3- (3,5-dimethoxyphenyl) -phenyl acrylamide (AL-017) Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and to explore its molecular mechanism. Methods: Mouse macrophages (RAW264.7) were cultured in vitro and stimulated with lipopolysaccharide (LPS). The effects of AL-017 on the release of nitric oxide (NO), total iNOS activity, iNOS and COX-2 mRNA expression, p38 signaling pathway whether or not affected. Results: AL-017 significantly inhibited the release of NO induced by LPS, decreased the activity of iNOS induced by LPS, significantly decreased the expression of iNOS and COX-2 mRNA induced by LPS, and significantly inhibited the LPS stimulation Phosphorylation of p38 mitogen-activated protein kinase (p38MAPK). Conclusion: AL-017 can effectively inhibit LPS-induced mouse macrophage inflammatory response, and its anti-inflammatory mechanism may be related to inhibition of p38MAPK phosphorylation.