【Animal modeling】-Effect of angiotensin (1-7) on the expression of GFAP, GDNF and cognitive function in the hippocampus of diabetic rats

  Objective: To observe the effect of angiotensin (1-7) [Ang (1-7)] on the expression of glial fibrillary acidic protein (GFAP), glial cell-derived neurotrophic factor (GDNF) and cognitive function in the hippocampus of diabetic rats. influence.

  Methods: Forty SD rats were randomly divided into normal control group (NC group), diabetes group (DM group), diabetes+Ang(1-7) group (DM1 group), diabetes+Ang(1-7)+A779 group (DM2 group). The diabetic rat model was established by intraperitoneal injection of STZ (60 mg/kg). The Morris water maze test was used to test the spatial learning and memory ability of the rats. RT-PCR and Western blot were used to detect the expression of GDNF mRNA and protein in the hippocampus, respectively. Nissl staining was used to observe The morphological changes of hippocampal neurons; the changes of GFAP and caspase-3 expression were detected by immunohistochemistry.

  Results: Compared with the NC group, the DM group had prolonged escape latency, decreased platform crossing times (P<0.05), decreased GDNF mRNA and protein expression in the hippocampus (P<0.05), and significantly damaged neurons (P<0.05). , GFAP expression decreased (P<0.05), and caspase-3 positive cells increased significantly (P<0.05). Compared with the DM group, the escape latency of rats in the DM1 group was shortened, the number of crossing platforms increased (P<0.05), the expression of GDNF in the hippocampus was increased (P<0.05), the neuron damage was decreased (P<0.05), and the expression of GFAP was increased (P<0.05). P<0.05), the expression of caspase-3 positive cells was significantly decreased (P<0.05), the combined application of Ang (1-7) and Mas receptor antagonist A779, the above effects of Ang (1-7) were blocked (P<0.05). 0.05).

  Conclusion: The combination of Ang(1-7) and Mas can improve the cognitive function of diabetic rats, and its mechanism may be related to up-regulating the expressions of GFAP and GDNF in the hippocampus of rats and affecting the survival of neurons.