Protective effect of apple (Ralls) polyphenol extract against aluminum-induced cognitive impairment and oxidative damage in rat

- Apple polyphenol extract (APE) markedly improved memory retention in Al-treated rat.
- APE attenuated Al-induced oxidative stress and histological degeneration.
- APE can decrease the level of Al and β-amyloid 42 in brain of the Al-treated rat.
- The neuroprotective role of APE against Al-toxicity involves chelation and antioxidant.

Aluminum (Al) has long been implicated in the pathogenesis of Alzheimer's disease (AD). Dietary polyphenols have been strongly associated with reduced risk of AD and the other nervous diseases. We aimed to evaluate the preventive effect of the apple polyphenol extract (APE) on Al-induced biotoxicity, in order to provide a new focus on the design of strategies to prevent AD and the other human diseases related to Al overload. Control, Al-treated (171.8 mg Al kg−1 day−1 10 weeks), APE + Al (Al-treatment as previously plus 200 mg kg−1 day−1 10 weeks), and group of APE per se were used. Al intake caused memory impairment, significant decrease of acetylcholinesterase, CK, SOD, CAT activity and the rate of ATP synthesis, increase the Al content, the level of malondialdehyde and β-amyloid42. Administration of APE significantly improved memory retention, attenuated oxidative damage, acetylcholinesterase activity and Al level in Al treated rats. Furthermore, chlorogenic acid (ChA) was used for analyzing stability of polyphenols-Al3+ complex. Log K1 was 10.51, and the mole ratio of Al3+ to ligand was 1:1. We further found that the amounts of Al increased significantly in feces of the rats gavaged with AlCl3 plus ChA compared with AlCl3. Our finding has shown APE has neuroprotective effects against Al-induced biotoxicity. Chelating with Al and disturbing its absorption could account for the neuroprotective roles of dietary polyphenols against Al toxicity.

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