Burstein S, Hunter S A, Sedor C, Shulman S
Biochem Pharmacol. 1982 Jul 15;31(14):2361-5. doi: 10.1016/0006-2952(82)90530-5.
Preliminary data [S. Burstein and S. A. Hunter, Biochem. Pharmac. 27, 1275 (1978)] showed that cannabinoids at levels of 1 microM or greater elevated the concentrations of prostaglandins in cell culture models. Further study [S. Burstein and S. A. Hunter, J. clin. Pharmac. 21, 240S (1981)] led to the suggestion that this effect was due to a stimulation of phospholipase A2 resulting in the release of free arachidonic acid which was then partly converted into the prostaglandin(s) normally synthesized by the particular target system. The present report gives detailed data on the cannabinoid-induced synthesis of prostaglandin E2 by te WI-38 fibroblast derived from human lung. The effect could be blocked by pretreatment with mepacrine, a phospholipase inhibitor, and aspirin, a cyclooxygenase inhibitor. These findings lend support to the hypothesis that some of the in vivo actions of the cannabinoids are due to modulations in prostaglandin synthesis at various tissue sites.
初步数据[S. 伯斯坦和S. A. 亨特,《生物化学与药理学》27,1275(1978)]表明,浓度为1微摩尔或更高的大麻素会提高细胞培养模型中前列腺素的浓度。进一步的研究[S. 伯斯坦和S. A. 亨特,《临床药理学杂志》21,240S(1981)]表明,这种效应是由于磷脂酶A2受到刺激,导致游离花生四烯酸释放,然后部分转化为特定靶系统通常合成的前列腺素。本报告给出了关于大麻素诱导人肺来源的WI - 38成纤维细胞合成前列腺素E2的详细数据。该效应可被磷脂酶抑制剂米帕林和环氧化酶抑制剂阿司匹林预处理所阻断。这些发现支持了这样一种假说,即大麻素在体内的某些作用是由于不同组织部位前列腺素合成的调节。