Improvement of naringein on cognition of model rats with Alzheimer's diseases and its mechanism
10.7501/j.issn.0253-2670.2013.06.016
- Author:
Wen-Qing YANG
1
Author Information
1. Neuroscience Research Center
- Publication Type:Journal Article
- Keywords:
Alzheimer's disease;
Amyloid β-protein;
Cognition;
Naringein;
Tau protein
- From:
Chinese Traditional and Herbal Drugs
2013;44(6):715-720
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect of naringein on the cognition of rats with Alzheimer's diseases (AD), its regulation on amyloid β-protein (Aβ) and Tau antibody, and its potential mechanism of improving the cognition of rats with AD. Methods: AD model of rats was established by intracerebroventricular (icv) Streptozotocin (STZ) on days 1 and 3, and then naringein and Rosiglitazone were ig administered. Rats in model and control groups were treated with the same volume of physiologic saline to induce dementia model. On day 21 after the first operation, spatial learning and memory of rats were tested in Morris water maze. The expression of insulin-degrading enzyme (IDE), glycogen synthase kinese-3β (GSK-3β), phospho-GSK-3β (pGSK-3β), Tau, and phospho-Tau (pTau) were measured by Western blotting. Aβ42 and Aβ40 levels in the brain of the AD rats were tested by immunohistochemistry. Results: Cognition of AD rats administered with naringein and Rosiglitazone could be recovered by Morris water maze (P < 0.05). Western blotting results showed that both naringein and Rosiglitazone could improve the expression of IDE and decrease the activity of GSK-3β, and reduce the phosphorylation level of Tau (P < 0.05). Immunohistochemistry demonstrated that the Aβ42 and Aβ40 in cerebral cortex of rats treated by naringein and Rosiglitazone were both decreased. Conclusion: Naringein as a peroxisome proliferator-activated receptor γ (PPARγ) excitomotor could act as insulin sensitizer, and could alleviate the cognition of AD rats, Aβ deposition, and phosphorylation of Tau through regulating the expression of insuline-related IDE and GSK-3β.
