Objective: To observe the expression and cognition of angiotensin (1-7) [Ang(1-7)] on glial fibrillary acidic protein (GFAP) and glial cell-derived neurotrophic factor (GDNF) in diabetic hippocampus Functional impact.
Methods: From the normal control group (NC group), diabetes group (DM group), diabetes + angiotensin (1-7) group (DM1 group), diabetes + angiotensin (1-7) + separate SD rats Randomly select 40 of them to enter A779. Group (DM2 group). Intraperitoneal injection of STZ (60 mg/kg) established a diabetic rat model. The Morris water maze test tested the spatial learning and memory abilities of rats. RT-PCR and Western blot were used to detect hippocampal GDNF mRNA expression and protein level. Observe the morphological changes of hippocampal neurons; immunohistochemical methods to detect changes in the expression of GFAP and caspase-3.
Results: Compared with the NC group, rats in the DM group had a longer escape latency, fewer crossing platforms (P\u003c0.05), and decreased GDNF mRNA and protein expression in the hippocampus (P\u003c0.05). (U003c0.05), the neuron is severely damaged. (P\u003c0.05), GFAP expression decreased (P\u003c0.05), and caspase-3 positive cells increased significantly (P\u003c0.05). Compared with the DM group, rats in the DM1 group had shorter escape latency, longer platform crossing time (P\u003c0.05), increased hippocampal GDNF expression (P\u003c0.05) and decreased neuronal damage (P\u003c0). 05), increased the expression of GFAP (P\u003c0.05), and significantly reduced the expression of caspase-3 positive cells (P\u003c0.05). After the combined administration of Ang (1-7) and Mas receptor antagonist A779, the above effects of Ang (1-7) were blocked. (P\u003c0.05).
Conclusion: The combination of Ang (1-7) and Mas can improve the cognitive function of diabetic rats. The mechanism is the up-regulation of GFAP and GDNF expression and neuronal survival in the hippocampus of rats.