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当前位置: 首页 > 文章 > γ-亚麻酸在RAW264.7细胞中的抗炎症作用机制 安徽农业科学 2010,38 (32) 18062-18063+18090
Position: Home > Articles > Anti-inflammatory Mechanism of γ-linolenic Acid in RAW264.7 Cells Journal of Anhui Agricultural Sciences 2010,38 (32) 18062-18063+18090

γ-亚麻酸在RAW264.7细胞中的抗炎症作用机制

作  者：
孔秀芹;殷志敏;罗兰
单  位：
南京师范大学生命科学学院江苏省分子医学生物技术重点实验室;南京大学生命科学学院医药生物技术国家重点实验室
关键词：
γ-亚麻酸;内毒素;炎症
摘  要：
[目的]探讨γ-亚麻酸(GLA)对脂多糖(LPS)诱导的RAW264.7细胞产生炎症介质的影响及其机制。[方法]以体外培养的巨噬细胞系RAW264.7细胞为研究对象,待细胞生长至融合状态后加入不同浓度(0、12.5、25、50μmol/L)的GLA预孵4 h,利用100 ng/m l的脂多糖(LPS)刺激12.0 h或0.5 h,同时设空白对照和LPS对照,利用蛋白印迹法检测诱生型一氧化氮合酶(iNOS)、环加氧酶-2(COX-2)蛋白的表达以及对IκBα、p-JNK/SAPK(Thr183/Tyr185)、p38 MAPK、p-p38 MAPK(Thr 180/Tyr182)、ERK1/2、p-ERK1/2的影响。[结果]GLA可以显著抑制LPS诱导的RAW264.7细胞中iNOS和COX-2的蛋白表达(P<0.05),且在0~50μmol/L GLA浓度范围内存在剂量依赖关系。GLA可以显著抑制IκBα的降解(P<0.05),从而抑制NFκ-B的激活。GLA可以显著抑制LPS诱导的JNK1/2以及ERK1/2的磷酸化(P<0.05),对p38的磷酸化没有显著影响。[结论]GLA具有很好的消炎功效。抑制JNK1/2和ERK1/2的磷酸化、抑制NF-κB的激活可能是GLA发挥生物学效应的重要机制。
译  名：
Anti-inflammatory Mechanism of γ-linolenic Acid in RAW264.7 Cells
作  者：
KONG Xiu-qin et al(Jiangsu Province Key Laboratory for Molecular and Medical Biotechnology,College of Life Sciences,Nanjing Normal University,Nanjing,Jiangsu 210097)
关键词：
Gamma-linolenic acid;Endotoxin;Inflammation
摘  要：
[Objective] The aim was to investigate the anti-inflammatory effect and the mechanism of gamma-linolenic acid on lipopolysaccharide-induced RAW264.7 cells.[Method] Macrophagic system RAW 264.7 cells were cultured in vitro,when cells grew to fusion state,they were pretreated with 0,12.5,25.0,50.0 μmol/L of GLA for 4 h,and then 100 ng/ml of LPS were added to induce for 12 h or 30 min.Meanwhile,the blank control and LPS control were set.And the expression of iNOS,COX-2 and the effect of GLA on IκBα,p-JNK/SAPK(Thr183/Tyr185),p38 MAPK,p-p38 MAPK(Thr180/Tyr182),ERK1/2,p-ERK1/2 were detected by Western blot.[Result] GLA significantly inhibited the expression of iNOS and COX-2 in RAW264.7 cells induced by LPS,in the range of 0-50 μmol/L of GLA,the concentration-dependent was existed(P<0.05).GLA could significantly inhibited the degradation of IκBα(P<0.05),thereby inhibited the activation of NF-κB.GLA could significantly inhibited the phosphorylation of LPS-induced JNK1/2 and ERK1/2(P<0.05),while it had not significantly effect on the phosphorylation of p38(P<0.05).[Conclusion] GLA had excellent anti-inflammation effect.The inhibition of the phosphorylation of JNK1/2,ERK1/2 and the inhibition of activation of NF-κB might be the important mechanism for the educing of its biological effect.

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