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川芎嗪对脂多糖诱导内皮细胞花生四烯酸通路炎症反应的影响 被引量:7

Antiatherosclerosis induced by ligustrazine against LPS through arachidonic acid signaling pathway
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摘要 目的研究川芎嗪对脂多糖(LPS)诱导内皮细胞花生四烯酸(AA)通路炎症反应的影响,为拓展川芎嗪临床适应症提供实验依据。方法在LPS(1 mg.L-1,2 h)诱导的原代培养人冠脉内皮细胞上,观察川芎嗪(1和10μmol.L-1,6 h)对COX-2、5-LOX和FLAP蛋白表达的影响;并观察加入LPS同时给予p-p38MAPK抑制剂SB203580(20μmol.L-1,6 h)或JAK2抑制剂AG490(20μmol.L-1,6 h)对上述蛋白表达及p-p38MAPK或p-STAT3蛋白表达的影响。结果川芎嗪可抑制COX-2、5-LOX和FLAP蛋白表达,抑制MAPK和STAT3通路磷酸化激活。结论川芎嗪靶向内皮细胞,抑制AA通路炎症反应,抑制MAPK和JAK2/STAT3通路激活。 Aim To examine the antiatherosclerotic effects induced by ligustrazine(LIG) against LPS.Methods In in vitro experiments,human coronary aortic endothelial cells(HCAEC)were treated with LPS(1 mg·L-1,2 h) to mimic in vivo atherosclerosis.Further investigation had been carried out through examining the effects of LIG(1 and 10 μmol·L-1) on protein expression of COX-2,5-LOX,FLAP and their related MAPK and JAK2/STAT3 signaling path-ways.Results LIG significantly decreased the protein expression of COX-2,5-LOX,FLAP at the concentrations of 1 and 10 μmol·L-1.The p-p38MAPK inhibitor SB203580 could antagonize the antiatherosclerotic effects induced by LIG.The phosphorylation of p38-MAPK and STAT3 had also been inhibited.Conclusion Antiatherosclerotic effects induced by LIG are targeting endothelial cells through inhibiting arachidonic acid-derived inflammation.
出处 《中国药理学通报》 CAS CSCD 北大核心 2012年第4期563-567,共5页 Chinese Pharmacological Bulletin
关键词 内皮细胞 动脉粥样硬化 川芎嗪 脂多糖 花生四烯酸 MAPK通路 JAK2/STAT3通路 endothelial cells atherosclerosis ligustrazine LPS arachidonic acid MAPK pathway JAK 2 / STAT 3 pathway
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