TY -的盟元,彭盟——张,剑盟-李,梁盟歌,Zhendi PY - 2019 DA - 2019/07/16 TI -氟西汀的焦虑行为糖尿病大鼠体外实验中通过减轻炎症SP - 4315038六世- 2019 AB -糖尿病(DM)患者的风险增加焦虑。高焦虑水平也显示增加糖尿病患者的压力,这可能会导致糟糕的临床结果。焦虑障碍的机制发展糖尿病患者仍然未知。因此,没有可用的治疗方法。在这里,我们测试的假设在DM小鼠的海马区胶质细胞可能负责他们的焦虑行为。此外,我们假定与抗抑郁治疗,氟西汀,可以减少焦虑失调的行为,防止胶质细胞在DM小鼠(少突细胞和星形胶质细胞)。糖尿病小鼠接种单一注射链脲霉素(STZ),其次是与氟西汀治疗。老鼠然后测试Y迷宫,空旷的田野,黑暗与光明的过渡,提升+迷宫测试测量的状态焦虑和认知。完成这些行为测试之后,老鼠牺牲和免疫印迹被用来检测海马组织的制造商少突细胞与星形胶质细胞相互作用的蛋白质。重点是针对成人少突细胞前体细胞(信息公开化)及其标记蛋白质来衡量其增殖和分化。 We found that fluoxetine could effectively mitigate the level of anxiety and attenuate the cognitive dysfunction in diabetic mice. Meanwhile, fluoxetine inhibited astrocyte activation in mice exposed to STZ, prevented the loss of myelin basic protein (MBP), and affected the function of OPCs in these diabetic mice. The results suggested that the changes of these glial cells in the brains of diabetic mice might be related to the high anxiety levels and cognitive deficit in DM mice. Fluoxetine could ameliorate the high anxiety level and prevent cognitive deficit via inhibiting astrocyte activation and repairing the oligodendrocyte damage. SN - 0962-9351 UR - https://doi.org/10.1155/2019/4315038 DO - 10.1155/2019/4315038 JF - Mediators of Inflammation PB - Hindawi KW - ER -