Yan C, Feng Y
Institute of Materia Medica, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100050.
Yao Xue Xue Bao. 1998 Dec;33(12):881-5.
The effects of 3-n-butylphthalide(NBP) on the levels of 6-keto-PGF1 alpha, TXB2 and 6-keto-PGF1 alpha/TXB2 ratio were studied with methods of RIA. d-NBP and l-NBP(0.1-100 mumol.L-1) concentration-dependently increased 6-keto-PGF1 alpha release, decreased TXB2 release from neuronal cells, and significantly enhanced extracellular 6-keto-PGF1 alpha/TXB2 ratio in primary cultured rat cortical neurons exposed to hypoxic-hypoglycemic media for 5 h or hypoxic-hypoglycemic media for 5 h following normal media for 3 h. Aspirin(0.1-100 mumol.L-1) was also shown to inhibit TXB2 release from cortical neurons in a dose-dependent manner. However aspirin only increased 6-keto-PGF1 alpha/TXB2 ratio at low dose because aspirin inhibited both 6-keto-PGF1 alpha and TXB2 release simultaneously at large dose(10-100 mumol.L-1). This suggests that the action of l-NBP, d-NBP and dl-NBP on the increase of 6-keto-PGF1 alpha/TXB2 ratio might be one of the mechanisms in which NBP enhanced focal cerebral blood flow and improved ischemic brain damage.
采用放射免疫分析法研究了3-正丁基苯酞(NBP)对6-酮-前列腺素F1α、血栓素B2水平及6-酮-前列腺素F1α/血栓素B2比值的影响。右旋-NBP和左旋-NBP(0.1 - 100μmol·L-1)呈浓度依赖性增加原代培养的大鼠皮层神经元在暴露于缺氧缺糖培养基5小时或先在正常培养基培养3小时后再暴露于缺氧缺糖培养基5小时时6-酮-前列腺素F1α的释放,降低血栓素B2的释放,并显著提高细胞外6-酮-前列腺素F1α/血栓素B2比值。阿司匹林(0.1 - 100μmol·L-1)也呈剂量依赖性抑制皮层神经元血栓素B2的释放。然而,阿司匹林仅在低剂量时增加6-酮-前列腺素F1α/血栓素B2比值,因为大剂量(10 - 100μmol·L-1)时阿司匹林同时抑制6-酮-前列腺素F1α和血栓素B2的释放。这表明左旋-NBP、右旋-NBP和消旋-NBP增加6-酮-前列腺素F1α/血栓素B2比值的作用可能是NBP增加局部脑血流量和改善缺血性脑损伤的机制之一。