TY -的A2 -奥斯托夫斯基,罗伯特·李盟——Changxiang AU - Wang Xueqian盟——燕Juntang AU - Cheng Fafeng AU - Ma, Xiaona AU - Chen Congai AU - Wang Wei AU -王,庆国PY - 2020 DA - 2020/10/12 TI -胆酸体外神经与血管的保护单位对氧气和葡萄糖通过BDNF-TrkB Deprivation-Induced损伤信号通路SP - 1201624六世- 2020 AB -缺血性中风(是)可以破坏各种类型的大脑细胞在神经血管单元(NVU)在结构和功能水平。因此,NVU被认为是更全面的治疗目标。有必要开发药物针对多个机制和细胞类型NVU反对。胆汁酸作为一个组成部分,胆酸报道能够分散在磷脂影响,进一步穿过血脑屏障(BBB)。然而,施加影响胆酸(CA) NVU卒中后仍不明朗。基于我们之前的研究,我们建立和进一步补充的特点功能体外NVU模型及其oxygen-glucose剥夺和复氧(OGD / R)模型。然后,我们研究了CA的维护后体外NVU OGD / R,并进一步讨论了特定分子靶点CA中扮演了重要的角色。第一次,我们发现CA明显保持BBB的完整性,表达下调细胞凋亡,减轻氧化应激和炎症损伤后OGD / R。同时,CA明显增加脑源性神经营养因子(BDNF)的水平,这主要是由星形胶质细胞分泌,在coculture系统OGD / R。结果表明,CA TrkB的表达明显增加,PI3K / Akt, MAPK / Erk和分子在神经元。 These positive effects on the downstream proteins of BDNF were suppressed by treatment with ANA12 which is an inhibitor of TrkB. In conclusion, the present study demonstrates that CA exerted multiple protective effects on the NVU, mediated by increasing the release of BDNF and further stimulating the BDNF-TrkB-PI3K/Akt and BDNF-TrkB-MAPK/Erk signaling pathways in the context of OGD/R-induced injury. These findings indicate that CA possesses the effect of antagonizing multiple mechanisms of IS and protecting multiple cell types in NVU and may be useful as a treatment for IS. SN - 1942-0900 UR - https://doi.org/10.1155/2020/1201624 DO - 10.1155/2020/1201624 JF - Oxidative Medicine and Cellular Longevity PB - Hindawi KW - ER -