Involvement of prostaglandin transport system at the blood-brainbarrier in the drug-induced vascular disorder in the brain.

采用脑外排指数法，将前列腺素E2 （PGE2）从小鼠脑内清除，半衰期为12分钟。相比之下，PGE2增加了脑毛细血管内皮细胞的增殖，并从NASIDs介导的细胞毒性中略微恢复。这些结果表明血脑屏障外排运输系统参与了小鼠脑内PGE2的清除，提示PGE2刺激脑毛细血管内皮细胞的血管化和重塑，非甾体抗炎药本身对脑毛细血管内皮细胞具有显著的细胞毒性。因此，非甾体抗炎药介导的PGE2清除减少和对脑毛细血管内皮细胞的细胞毒性可能导致脑炎症中严重的血管增生。

Using Brain Efflux Index method, prostaglandin E2 (PGE2) was eliminated from mouse brain with a half-life of 12 minutes. By contrast, PGE2 increased brain capillary endothelial cell proliferation and slightly recovered from NASIDs mediated cytotoxicity. These results demonstrate that BBB efflux transport system is involved in the PGE2 clearance in mouse brain and suggest that PGE2 stimulate vascularization and remodeling of brain capillary endothelial cells and NSAIDs itself exert significantly cytotoxicity against brain capillary endothelial cells. Therefore, NSAIDs mediated reduction of PGE2 clearance and cytotoxicity against brain capillary endothelial cells may cause severe angiopacy in brain inflammation.