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Background: Numerous pieces of evidence support that oxidative stress is a key factor in the pathogenesis of neurodegenerative diseases, like Alzheimer’s Disease (AD). Suppression of oxidative stress is an attractive strategy and flavonoids as potent natural antioxidants are extremely noticeable. 
Objectives: In this study, the effects of Kaempferol (KMP) were evaluated on passive avoidance memory, hippocampal Nrf-2, and beclin-1 expression in a rat model of Aβ1-42 –induced AD.
Materials & Methods: Forty male Wistar rats weighing 200-250 g were divided into five groups (n=8); sham-operated, AD model, and KMP treatment (5, 7.5, 10 mg/kg, i.p. for three weeks). Animals received an intracerebroventricular injection of amyloid-beta (1-42) to establish an AD model. Passive avoidance memory of rats was evaluated using a shuttle box on day 21; Step-Through Latency (STL) and time spent in The Dark Compartment (TDC) were recorded. Then, hippocampus homogenates were used for biochemical and molecular analysis by real-time PCR, western blot, and ELISA.
Results: It was found that KMP improved memory evidenced by increased STL (P≤0.05) and decreased TDC (p≤0.01). KMP also increased the levels of Total Antioxidant Capacity (TAC) in the hippocampus of rats (P≤0.05). In addition, KMP enhanced the expression of Nrf-2 mRNA (P≤0.001) and beclin-1 protein in the hippocampus tissues (P≤0.001).
Conclusion: Overall, it is suggested that the memory-improving effect of KMP is mediated, at least in part, by enhancing Nrf-2 and TAC. KMP is also able to induce autophagy through the expression of beclin-1.

Keywords: Alzheimer’s disease, autophagy, Nrf-2 and, Kaempferol

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