Walnut Protein Hydrolysates Play a Protective Role on Neurotoxicity Induced by d-Galactose and Aluminum Chloride in Mice.

Li Feng,Huaide Xu,Yifan Nai,Fei Peng,Xiaojing Wang,Mei Li,Jianqiao Liao,Hongjie Lei

doi:10.3390/molecules23092308

Li Feng, Huaide Xu + Show 6 more

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https://doi.org/10.3390/molecules23092308

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Abstract

In recent years, with an increase in the aging population, neurodegenerative diseases have attracted more and more attention. This study aimed to investigate the potential neuroprotective effect of defatted walnut meal protein hydrolysates (DWMPH) on neurotoxicity induced by d-galactose (d-gal) and aluminum chloride (AlCl3) in mice. The animal models were established by combining treatments with d-gal (200 mg/kg/day, subcutaneously) and AlCl3 (100 mg/kg in drinking water) for 90 days. During the 90 days, 1 g/kg of DWMPH was administrated orally every day. The results indicated that DWMPH treatment alleviated oxidative stress, reversed cholinergic dysfunction, and suppressed the release of proinflammatory cytokines in the brains of d-gal + AlCl3-treated mice, and thus improving the learning and memory functions of these mice, which was closely correlated with the strong antioxidant activity of DWMPH. This finding suggests that DWMPH might be a promising dietary supplement in improving neuronal dysfunctions of the brain.

Highlights

It has been recognized that free radicals and oxidative stress play a vital role in neuronal degeneration, probably because the brain is more vulnerable to damage by oxidative stress than other organs, for its high rate of oxygen consumption, abundance of unsaturated lipids, and relatively lower availability of antioxidant enzymes [1,2]
We investigated the potential neuroprotective effect of defatted walnut meal protein hydrolysates (DWMPH) on neurotoxicity induced by D-gal and AlCl3 combination in Kunming mice, by examining the cognitive capacity of experimental mice and assessing the oxidative stress, cholinergic function, and neuroinflammatory of mice brains
The data were analyzed by one-way ANOVA using SPSS 18.0, and a least significant difference (LSD) range test was conducted to identify the significance of the differences (p < 0.05)

Summary

Introduction

It has been recognized that free radicals and oxidative stress play a vital role in neuronal degeneration, probably because the brain is more vulnerable to damage by oxidative stress than other organs, for its high rate of oxygen consumption, abundance of unsaturated lipids, and relatively lower availability of antioxidant enzymes [1,2]. Possible therapeutic and preventive strategies have always been attracted to the inhibition of oxidative stress and inflammation, which is based on their pivotal roles in the pathogenesis of neuronal degeneration. Chronic exposure to D-galactose (D-gal), which is widely used to establish a model of accelerated aging, could induce oxidative stress, influence neurogenesis, and result in neurodegeneration, similar to the natural aging in mice [6]. Aluminum, a neurotoxic agent, could induce cholinergic dysfunction in the CNS and the generation of free radicals and neurotoxicity in the brain [7,8]. Mice administered with 60 mg/kg D-gal and 10 mg/kg aluminum chloride (AlCl3 ) intraperitoneally for 40 days eventually led to an abnormal cholinergic system, oxidative stress, neuronal apoptosis, and neuroinflammation, accompanied by cognitive impairment [9].

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