农业科学与技术（英文版）
農業科學與技術（英文版）
농업과학여기술（영문판）
AGRICULTURAL SCIENCE & TECHNOLOGY
2010年
6期
1-3
,共3页
γ-亚麻酸%内毒素%炎症
γ-亞痳痠%內毒素%炎癥
γ-아마산%내독소%염증
Gamma-linolenic acid%Endotoxin%Inflammation
[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]采用体外培养的巨噬细胞系RAW264.7细胞,待细胞生长至融合状态后加入不同浓度(0、12.5、25、50 μmol/L)的GLA预孵4 h,利用100 ng/ml的脂多糖(LPS)刺激12 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0～50 μmol/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NF-κB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的磷酸化没有显著的影响.[结论]GLA具有很好的消炎功效.抑制JNK1/2以及ERK1/2的磷酸化、抑制NF-κB的激活可能是其发挥生物学效应的重要机制.
[目的]探討γ-亞痳痠(GLA)對脂多糖(LPS)誘導的RAW264.7細胞產生炎癥介質的影響及其機製.[方法]採用體外培養的巨噬細胞繫RAW264.7細胞,待細胞生長至融閤狀態後加入不同濃度(0、12.5、25、50 μmol/L)的GLA預孵4 h,利用100 ng/ml的脂多糖(LPS)刺激12 h或0.5 h,同時設空白對照和LPS對照,利用蛋白印跡法檢測誘生型一氧化氮閤酶(iNOS)、環加氧酶-2(COX-2)蛋白的錶達以及對IκBα、p-JNK/SAPK(Thr183/Tyr185)、p38 MAPK、p-p38 MAPK(Thr 180/Tyr182)、ERK1/2、p-ERK1/2的影響.[結果]GLA可以顯著抑製LPS誘導的RAW264.7細胞中iNOS和COX-2的蛋白錶達(P＜0.05),且在0～50 μmol/L GLA濃度範圍內存在劑量依賴關繫.GLA可以顯著抑製IκBα的降解(P＜0.05),從而抑製NF-κB的激活.GLA可以顯著抑製LPS誘導的JNK1/2以及ERK1/2的燐痠化(P＜0.05),對p38的燐痠化沒有顯著的影響.[結論]GLA具有很好的消炎功效.抑製JNK1/2以及ERK1/2的燐痠化、抑製NF-κB的激活可能是其髮揮生物學效應的重要機製.
[목적]탐토γ-아마산(GLA)대지다당(LPS)유도적RAW264.7세포산생염증개질적영향급기궤제.[방법]채용체외배양적거서세포계RAW264.7세포,대세포생장지융합상태후가입불동농도(0、12.5、25、50 μmol/L)적GLA예부4 h,이용100 ng/ml적지다당(LPS)자격12 h혹0.5 h,동시설공백대조화LPS대조,이용단백인적법검측유생형일양화담합매(iNOS)、배가양매-2(COX-2)단백적표체이급대IκBα、p-JNK/SAPK(Thr183/Tyr185)、p38 MAPK、p-p38 MAPK(Thr 180/Tyr182)、ERK1/2、p-ERK1/2적영향.[결과]GLA가이현저억제LPS유도적RAW264.7세포중iNOS화COX-2적단백표체(P＜0.05),차재0～50 μmol/L GLA농도범위내존재제량의뢰관계.GLA가이현저억제IκBα적강해(P＜0.05),종이억제NF-κB적격활.GLA가이현저억제LPS유도적JNK1/2이급ERK1/2적린산화(P＜0.05),대p38적린산화몰유현저적영향.[결론]GLA구유흔호적소염공효.억제JNK1/2이급ERK1/2적린산화、억제NF-κB적격활가능시기발휘생물학효응적중요궤제.
[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, and in the range of 0-50 μmol/L of GLA, the inhibition effect was concentration-dependent (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.
