Spatz M, Stanimirovic D, Uematsu S, Roberts L J, Bembry J, McCarron R M
Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Prostaglandins Leukot Essent Fatty Acids. 1993 Oct;49(4):789-93. doi: 10.1016/0952-3278(93)90027-t.
Endothelial cells derived from human brain capillaries (HBCEC) synthesize prostaglandin D2 (PGD2) which can be stimulated, among other prostanoids, by endothelin 1 (ET-1). Both the PGD2 induced by ET-1 and the exogenously added PGD2 to HBCEC are converted to 9 alpha, 11 beta-prostaglandin F2 (9 alpha, 11 beta-PGF2), a known potent vasoconstrictor. Exogenous PGD2 also dose-dependently enhanced the production of vasoconstrictive PGF2 alpha, thromboxane B2 (TXB2), and the vasodilatory PGE2 as well as cAMP by HBCEC. The PGD2-induced formation of PGF2 alpha, PGE2, and TXB2 was reduced by the cyclooxygenase inhibitors acetylsalicylic acid (ASA) or indomethacin (Indo), indicating for the first time that PGD2 may contribute to the formation of prostanoids in HBCEC. These results strongly suggest that PGD2 may play an important role in the regulation of cerebral capillary function under physiologic and pathologic conditions.
源自人脑微血管的内皮细胞(HBCEC)可合成前列腺素D2(PGD2),在内皮素1(ET-1)等其他类前列腺素的作用下,PGD2的合成可被刺激。ET-1诱导产生的PGD2以及向HBCEC中添加的外源性PGD2均可转化为9α,11β-前列腺素F2(9α,11β-PGF2),这是一种已知的强效血管收缩剂。外源性PGD2还能剂量依赖性地增强HBCEC产生血管收缩性的PGF2α、血栓素B2(TXB2)以及血管舒张性的PGE2和cAMP。环氧化酶抑制剂乙酰水杨酸(ASA)或吲哚美辛(Indo)可减少PGD2诱导的PGF2α、PGE2和TXB2的形成,这首次表明PGD2可能参与HBCEC中类前列腺素的形成。这些结果有力地表明,PGD2可能在生理和病理条件下对脑微血管功能的调节中发挥重要作用。