| Popis: |
Cognitive dysfunction is a serious neurological complication of diabetes mellitus (DM). Recent studies have found that in addition to the hippocampus, the cerebellum is also involved in regulating cognitive functions such as learning and memory through long-term depression (LTD), but the molecular mechanism of cognitive impairment resulted from cerebellum dysfunction in diabetes has not been fully elucidated. Moreover, gastrodin has been supposed to reduce the incidence of Alzheimer's disease and improve function in the central nervous system. This study aimed to evaluate the changes of LTD-related factors including GluR2, p-GluR2, PKC, BDNF, and TrkB in the cerebellar cortex of diabetic rats by western blotting and double immunofluorescence, and to explore the therapeutic effect of gastrodin. We found that there was neuronal necrosis and neuronophagia in the cerebellar cortex of diabetic rats, the protein expression levels of GluR2 and PKC in Purkinje cells were significantly decreased, and p-GluR2, BNDF and TrkB were significantly increased. After treatment with gastrodin, the damage of Purkinje cells was ameliorated, and the expression of the above factors was restored to a certain extent. Arising from the above, Thus, diabetes may cause cerebellar LTD by affecting the internalization of GluR2, thereby causing cognitive dysfunction. Gastrodin ameliorates cerebellar neuronal damage and restores the expression levels of GluR2 and BDNF in diabetic rats. |
