摘要
目的观察N-araehidonoyl ethanolamide（Anandamide，AEA）对A549细胞的作用并且探讨AEA的作用机制。方法倒置显微镜观察细胞的形态学变化，并用MTT法考察细胞增殖情况。结果AEA引起A549细胞死亡，且呈现剂量依赖性，IC50为（50．90±11．27）wmol·L^-1。A549细胞上表达有辣椒素受体（vanilloidreceptor1，VRl），AEA对A549的作用，不可以被VRl特异性的拮抗剂Capsazepine（-10μmol·L^-1）和RutheniumRea（-10μmol·L^-1）所拮抗。但AEA的作用可以被阿司匹林所减轻（P〈0．05或P〈0．01）。结论①AEA引起A549细胞死亡并不依赖VRl。②AEA的环氧化酶代谢产物Prostaglandin-ethanolamide（SPG-EAs）有可能参与该过程。
Aim The effect of N-arachidonoyl ethanolamide （ Anandamide, AEA ） cancer cell A549 was analysed , on the human lung the possible mechanism was detected. Methods To assess the sensitivity of A549 to AEA, A549 cells were exposed to increasing doses of AEA with or without the antagonists to vanilloid receptor 1 （VR1） and aspirin. MTT methods were employed to investigate A549 cell proliferation. Results A549 cells exhibited dose-dependent sensitivity to AEA resulting in dramatic cell death. But the effect of AEA on A549 could not be antagonized by the antagonists such as capsazepine and Ruthenium Red. However, cyclooxygenase （COX） inhibitor, aspirin, could attenuate A549 cell death caused by AEA （P 〈 0.05 or P 〈 0.01 ）. Conclusions The inhibition on A549 caused by AEA might be via COX pathway, not depending on VR1, and the metabolic product PG-EAs might be involved in this process.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2008年第5期663-666,共4页
Chinese Pharmacological Bulletin
