Abstract

Objective (s)Accumulating evidence has suggested that oxidative stress and apoptosis are involved in the aging process. d‐galactose (gal) has been reported to cause symptoms of aging in mice, accompanied by liver and brain injuries. Our present work was to study the potential antioxidative and anti‐apoptotic effects of walnut and to explore how these effects act on mice in a d‐gal‐induced aging model.Materials and MethodsAging mice were induced by subcutaneous injection of d‐gal (200 mg kg−1 d−1 for 8 weeks). Walnut samples were simultaneously administered to the d‐gal‐induced aging mice once daily by intragastric gavage. Finally, body weight, organ index, cognitive function, levels of antioxidative enzymes, and liver function were monitored.ResultsThe kernel pellicles of walnut could not only improve the learning and memory ability, and the organ index, but also significantly decrease body weight and normalize the levels of activity of antioxidative enzymes in aging mice. Further, the walnut seed coat would protect damages of hippocampus and liver in aging mice.HighlightsIn the current study, we investigated the effects of walnut kernels and walnut seed coats (WSCs) on d‐galactose‐induced aging mice. WSC was firstly found to have beneficial effects on d‐gal‐treated mouse's brain with learning and memory impairment, which probably through the underlying mechanism reduces oxidative damage and limits neuroinflammation. In addition, WSC had a protective effect on liver damage in d‐galactose sensing mice.

Highlights

  • Aging is a major factor involved in neurological impairments, decreased anti­oxidant activities, and enhanced neuroinflammation (Rehman, Shah, Ali, Chung, & Kim, 2017)

  • In comparison with the model group, the walnut seed coats (WSCs) and Vitamin E (VE) groups could prolong the number of errors reduced and the time to jump off the platform (p < 0.05 for all), and reduce the finding the latency of the platform times (p < 0.05 for all)

  • We aimed to demonstrate that during a period of 8 weeks of aging model establishment via subcutaneous injection of d-­gal in mice, WSC and walnut seed (WS) could protect against d-­gal-­induced organ injury in vivo

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Summary

Introduction

Aging is a major factor involved in neurological impairments, decreased anti­oxidant activities, and enhanced neuroinflammation (Rehman, Shah, Ali, Chung, & Kim, 2017). Aging and related diseases is a significant challenge for medical gerontology (Kennedy & Pennypacker, 2014). D-­galactose administration has been shown to induce impairments in memory and cognition in mice accompanied by aging-­ associated deficits. The d-­gal exposure could exacerbate oxidative damage, including increased content of malondialdehyde (MDA), and decreased total anti­oxidative capabilities (AOCs), total superoxide dismutase (SOD), and glutathione peroxidase (GSH-­Px) activities (Yin et al, 2010).

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