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Walnut (Juglans regia) Peptides Reverse Sleep Deprivation-Induced Memory Impairment in Rat via Alleviating Oxidative Stress
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2018-09-18 00:00:00 , DOI: 10.1021/acs.jafc.8b03884
Shuguang Wang 1, 2 , Guowan Su 1, 2 , Qi Zhang 1, 2 , Tiantian Zhao 1, 2 , Yang Liu 1, 2 , Lin Zheng 1 , Mouming Zhao 1, 2, 3
Affiliation  

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.

中文翻译:

核桃(胡桃)肽通过减轻氧化应激逆转大鼠睡眠剥夺所致的记忆障碍。

这项研究的目的是确定核桃蛋白水解物(WPH)对大鼠睡眠剥夺(SD)诱导的记忆缺陷的神经保护作用,并进一步鉴定和表征针对谷氨酸诱导的PC12细胞凋亡的有效神经保护肽。结果表明,在莫里斯水迷宫测试中,对于WPH及其低分子量分数WPHL,尤其是WPHL,观察到了对行为表现的显着改善作用。此外,口服WPH和WPHL后,大鼠脑部的抗氧化防御能力降低(过氧化氢酶,谷胱甘肽过氧化物酶(GSH-px)和超氧化物歧化酶(SOD))和SD引起的丙二醛含量增加均达到正常。然后从WPHL中鉴定了三种神经保护肽,包括GGW,VYY和LLPF,与谷氨酸组48.61±3.99%相比,它可以保护PC12细胞免受谷氨酸诱导的细胞凋亡,相对细胞存活率分别为78.29±3.09%,80.65±1.74%和83.97±3.06%。它们对GGW和VYY的保护作用的潜在机制可能与它们强大的自由基清除活性以及降低PC12细胞中活性氧的产生以及SOD和GSH-px耗竭的能力有关。值得注意的是,LLPF的显着神经保护作用(在体外未显示出明显的自由基清除活性)可归因于其对Ca的抑制作用。它们对GGW和VYY的保护作用的潜在机制可能与它们强大的自由基清除活性以及降低PC12细胞中活性氧的产生以及SOD和GSH-px耗竭的能力有关。值得注意的是,LLPF的显着神经保护作用(在体外未显示出明显的自由基清除活性)可归因于其对Ca的抑制作用。它们对GGW和VYY保护作用的潜在机制可能与它们强大的自由基清除活性以及降低PC12细胞中活性氧的产生以及SOD和GSH-px消耗的能力有关。值得注意的是,LLPF的显着神经保护作用(在体外未显示出明显的自由基清除活性)可归因于其对Ca的抑制作用。2+内流和线粒体膜电位崩溃。此外,所有这些肽均可调节凋亡相关蛋白(Bax和Bcl-2)的表达。因此,核桃肽可能被认为是对抗与记忆缺陷有关的神经退行性疾病的潜在保健品。
更新日期:2018-09-18
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