| Objective To investigate the role and mechanism of autophagy in prefrontal neuronal damage in diabetes,depression and diabetic comorbid depression.Methods 1.Forty male Wistar rats were randomly selected and randomly divided into normal control group(CON),depression group(D),diabetes group(DM)and diabetes comorbid depression group(DD)by chronic unpredictable stress stimulation and high-fat feeding.The stress level of rats was detected by open field experiments and forced swimming experiments.Diabetes mellitus in rats was detected by detecting changes in blood glucose and body weight.HE staining,Niselferi staining,immunohistochemistry,immunofluorescence and West blotting were used to detect the differences in the expression of LC3,Beclin-1 and P62 autophagy-related factors between the groups.At the same time,the expression of PI3K/AKT/MTOR protein in the autophagy-related pathway was examined.Results Animal experiment results: HE staining results showed that the damage of neurons in each group in the prefrontal region of rats was not obvious,and the degree of neuron edema in group D and DM group was slightly increased compared with that in CON group.The results of Nissl staining also confirm this.The results of Western Blot showed that the autophagy-related protein LC3 Belin-1 had different degrees of increase compared with the control group,and the DD group was the most obvious.The results of tissue immunofluorescence staining showed that the expression level of autophagyrelated protein was corroborated with the results of Western Blot experiment.Conclusion Diabetic comorbid depression can have abnormal morphological changes in rat prefrontal cortex neurons and PC12 cells,which may be the basis of their damage;Diabetic comorbid depression neuronal damage is associated with increased autophagy;PI3K/AKT/mTOR signaling pathway inhibition is involved in the regulation of neuronal autophagy in diabetic comorbid depression. |
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