Study2018

Walnut ( Juglans regia) Peptides Reverse Sleep Deprivation-Induced Memory Impairment in Rat via Alleviating Oxidative Stress

Wang S, Su G, Zhang Q, Zhao T, Liu Y, Zheng L, Zhao M

Journal of agricultural and food chemistry · 58 citations

How it was studied

Design
Animal study (classified by our AI screen)
Studied in
People, plus animal or lab work
Main outcome
Health markers and function

Who paid for it

Funding
Independent funding
Government
Ministry of Science and Technology of the People's Republic of China
Government
Government of Guangdong Province
Government
Ministry of Human Resources and Social Security
Government
Guangzhou Science and Technology Plan Projects
Government
Ministry of Science and Technology of the People's Republic of China
Grants
Government of Guangdong Province (2016TQ03N728); Ministry of Human Resources and Social Security (BX201700081); Ministry of Science and Technology of the People's Republic of China (2017YFD0400201)

Based on 5 listed funder(s).

Publication

Published
2018-09-18 · J Agric Food Chem · vol. 66 · issue 40 · pp. 10617–10627
Publisher
American Chemical Society
Cited
91 citations · more than 87% of similar papers · 1.9× the field average
References
48 works
Access
Paywalled
Research areas
Protein Hydrolysis and Bioactive Peptides · Biochemical effects in animals · Fatty Acid Research and Health
Keywords
Neuroprotection, Oxidative stress, Superoxide dismutase, Malondialdehyde, Glutathione peroxidase, Pharmacology, Chemistry, Antioxidant, Glutamate receptor, Biochemistry, Reactive oxygen species, Glutathione, Viability assay, Apoptosis, Biology, Enzyme
MeSH
pc12 cells, animals, humans, rats, juglans, sleep deprivation, reactive oxygen species, malondialdehyde, catalase, glutathione peroxidase, superoxide dismutase, peptides, neuroprotective agents, memory, apoptosis, oxidative stress, female, male, membrane potential, mitochondrial

7 authors

From CN

  • Shuguang WangSouth China University of Technology
  • Guowan SuSouth China University of Technology
  • Qi ZhangSouth China University of Technology
  • Tiantian ZhaoSouth China University of Technology
  • Yang LiuSouth China University of Technology
  • Lin Ping Zheng · correspondingSouth China University of Technology

Abstract

The aim of this study was to determine the neuroprotective effects of walnut protein hydrolysates (WPH) against memory deficits induced by sleep deprivation (SD) in rat and further to identify and characterize the potent neuroprotective peptides against glutamate-induced apoptosis in PC12 cells. Results showed that a remarkable amelioration effect on behavioral performance in Morris water maze test was observed for WPH and its low molecular weight fraction WPHL, especially for WPHL. Additionally, a reduction of antioxidant defense (catalase, glutathione peroxidase (GSH-px), and superoxide dismutase (SOD)) and an increase of malondialdehyde content induced by SD were normalized in brain of rat after oral administration of WPH and WPHL. Then three neuroprotective peptides including GGW, VYY, and LLPF were identified from WPHL, which could protect PC12 cells against glutamate-induced apoptosis with relative cell viability of 78.29 ± 3.09%, 80.65 ± 1.74%, and 83.97 ± 3.06%, respectively, versus glutamate group 48.61 ± 3.99%. The possible mechanism underlying their protective effects of GGW and VYY could be related to their strong radical scavenging activity as well as their ability to reduce reactive oxygen species production and the depletion of SOD and GSH-px in PC12 cells. Notably, the marked neuroprotective effects of LLPF, which did not show obvious free-radical scavenging activity in vitro, could be attributed to its strong effects on inhibiting Ca2+ influx and mitochondrial membrane potential collapse. Additionally, all these peptides could regulate the expression of apoptosis-related proteins (Bax and Bcl-2). Therefore, walnut peptides might be regarded as the potential nutraceuticals against neurodegenerative disorders associated with memory deficits.

Abstract via Europe PMC. Copyright remains with the authors or publisher.

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