盖雅婷, 舒强, 陈彩霞, 赖幼琳, 李文君, 彭璐, 林丽敏, 金鑫. 大麻素受体2在油酰乙醇胺抗动脉粥样硬化中的作用J. 药学学报, 2014,49(3): 316-321.
引用本文: 盖雅婷, 舒强, 陈彩霞, 赖幼琳, 李文君, 彭璐, 林丽敏, 金鑫. 大麻素受体2在油酰乙醇胺抗动脉粥样硬化中的作用J. 药学学报, 2014,49(3): 316-321.
GAI Ya-ting, SHU Qiang, CHEN Cai-xia, LAI You-lin, LI Wen-jun, PENG Lu, LIN Li-min, JIN Xin. Anti-atherosclerosis role of N-oleoylethanolamine in CB2J. Acta Pharmaceutica Sinica, 2014,49(3): 316-321.
Citation: GAI Ya-ting, SHU Qiang, CHEN Cai-xia, LAI You-lin, LI Wen-jun, PENG Lu, LIN Li-min, JIN Xin. Anti-atherosclerosis role of N-oleoylethanolamine in CB2J. Acta Pharmaceutica Sinica, 2014,49(3): 316-321.

大麻素受体2在油酰乙醇胺抗动脉粥样硬化中的作用

Anti-atherosclerosis role of N-oleoylethanolamine in CB2

  • 摘要: 观察PPAR-α激动剂油酰乙醇胺(N-oleoylethanolamine,OEA)对人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)抗炎相关受体大麻素受体2(cannabinoid receptor 2,CB2)的作用。从新生儿脐带中提取HUVECs,给予不同剂量OEA,RT-PCR及Western blotting检测CB2基因和蛋白表达。采用PPAR-α阻断剂MK886或CB2阻断剂AM630分别阻断PPAR-α或CB2信号通路,给药组和阻断剂组给予OEA,用TNF-α诱 导模型组、给药组和阻断剂组炎症产生,Western blotting法测定各组VCAM-1蛋白表达或进行THP-1黏附实验。结果表明,OEA(10和50 μmol·L-1)组的CB2表达上升,100 μmol·L-1 OEA组较空白组无明显变化;OEA抑制VCAM-1蛋白表达及THP-1细胞黏附;分别给予PPAR-α、CB2阻断剂MK886/AM630后,OEA对VCAM-1及单核细胞黏附的抑制作用明显降低。结果提示,OEA可能通过激活CB2通路起到抗动脉硬化的作用。

     

    Abstract: To observe a PPAR-α agonist effect of N-oleoylethanolamine (OEA) on CB2 (cannabinoid receptor 2), an anti-inflammatory receptor in vascular endothelial cell, healthy HUVECs and TNF-α induced HUVECs were used to establish a human vascular endothelial cell inflammatory model. Different doses of OEA (10, 50 and 100 μmol·L-1) had been given to HUVECs, cultured at 37 ℃ for 7 h and then collected the total protein and total mRNA. CB2 protein expression was detected by Western blotting and CB2 mRNA expression was assayed by real-time PCR. As the results shown, OEA (10 and 50 μmol·L-1) could induce the CB2 protein and mRNA expression, but not 100 μmol·L-1. To detect if anti-inflammation effect of OEA is partly through CB2, CB2 inhibitor AM630 was used to inhibit HUVEC CB2 expression, then the VCAM-1 expression induced by TNF-α was detected, or THP-1 adhere to TNF-α induced HUVECs was examined. OEA (50 μmol·L-1) could inhibit TNF-α induced VCAM-1 expression and THP-1 adhere to HUVECs, these effects could be partly inhibited by a CB2 inhibitor AM630. The anti-inflammation effect of OEA is induced by PPAR-α and CB2, suggesting that CB2 signaling could be a target for anti-atherosclerosis, OEA have wide effect in anti-inflammation, it may have better therapeutic potential in anti-inflammation in HUVECs, thus achieving anti-atherosclerosis effect.

     

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