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Protective Effect of IGF-1 Pathway Hippocampus of Diabetic Encephalopathy Rats

Author: HuYiPing
Tutor: WeiZuoPing
School: Chongqing Medical University
Course: Geriatrics
Keywords: Diabetic encephalopathy cognitive deficits IGF-1 IGF-1R curcumin
CLC: R285.5
Type: Master's thesis
Year: 2011
Downloads: 202
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Abstract


BackgroundDiabetes is associated with gradually developing damage in the central nervous system by glucose metabolic disorders. Diabetic encephalopathy, characterized by impaired cognitive functions and structural abnormalities, is recognized as a complication of diabetes. It was proposed firstly by the Nielsen in 1965. However, its pathogenesis is still unknown. In recent years, considerable progress has been made toward understanding the biochemical mechanisms leading to diabetic encephalopathy and found that IGF-1 signal pathway might be play an important role. There is not effective treatment on treatment of diabetic encephalopathy recently. So it is of great sigficance to study the mechanism and find effective drugs for treatment.Curcumin, derived from the rhizome of the herb Curcuma longa has been demonstrated as a strong candidate for the prevention and treatment of major disabling age-related neurodegenerative disorders. So we designed the study: we induced diabetic model to observe the effect of curcumin on cognitive function in diabetic encephalopathy rats and its mechanism of protection, to provide experimental basis for the clinical application.ObjectiveThis study aims to investigate the impacts of curcumin against cognitive deficits and to confirm the impact of curcumin on IGF-1 tentatively and the mechanism in order to furnish the theory foundation for the therapy of diabetic encephalopathy clinically.Method(1)Animals 40 three- month SD male rats, weight 200 ~ 250(g), were randomly divided into two groups: control group (n = 10) and diabetes group (n = 30). SD rats were injected STZ (60mg/kg) to establish diabetes model, then we used water maze test to select diabetes encephalopathy rats at 12 weeks. Control group rats were randomly divided into two groups: normal control group (A group, n = 5) and normal curcumin group (B group, n = 5).Model group rats were randomly divided into diabetes encephalopathy group (C group, n = 10) and curcumin treatment group (D group, n = 10).Normal curcumin group and curcumin treatment group were given curcumin 60mg/kg/d for 12 weeks .(2)Morris water maze test Each rats were respectively measured by the weight (g), blood glucose (mmol/L), escape latency (S) at 0 week, 12 week, 24 week and glycated hemoglobin (%) at 24 week.(3)Biochemical assays The rat were decapitated under anesthesia. Three animals per group were perfused with 4% paraformaldehyde. The whole brain was quickly removed and dissected into hippocampus and cleaned with chilled normal saline on the ice. The other hippocampus were dissected, snap-frozen in liquid nitrogen, and stored at -80℃for purification of RNA.Result(1)Diabetes encephalopathy rats became weak obviously after STZ injected for 12 weeks. There was marked decline in the body weights of STZ-treated rats as compared to age matched control rats .However,the modle group rats blood glucose levels were significantly increased compared to the control group rats. Curcumin treatment significantly improved body weights and the blood glucose levels of diabetes encephalopathy rats.(2) The cognitive deficit was preformed in the Morris water maze test. The mean escape latency was no difference between any of the groups at first of testing ,but there was significant difference between diabetic group rats (48.60±6.07)S and control group rats (23.70±3.94)S. Curcumin treatment significantly decreased mean transfer latency in diabetic animals.(3) Compared with the normal control group, cognitive function in the model rats significantly reduced. And the content of IGF-1、IGF-1R in the hippocampal of the model rats decreased obviously after the formation of models .However the expression of IGF-1、IGF-1R was markedly increased after the treatment of curcumin. Conclusion(1)STZ -induced diabetes produced marked impairment in cognitive function at 12 weeks, treatment with curcumin significantly ameliorated cognitive deficits.(2)The decreased expression of IGF-1 , IGF-1R in hippocampus neurons of the model rats might play an important role in the pathogenesis of diabetic encephalopathy. Protective effect of IGF-1 signal pathway in hippocampus possibly through the regulation of the expression level of IGF-1/IGF-1R of the modle rats.

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