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紫薯色素改善由D-半乳糖诱导的衰老小鼠大脑中的认知缺陷,并减轻氧化损伤和炎症。

Purple sweet potato color ameliorates cognition deficits and attenuates oxidative damage and inflammation in aging mouse brain induced by d-galactose.

作者信息

Shan Qun, Lu Jun, Zheng Yuanlin, Li Jing, Zhou Zhong, Hu Bin, Zhang Zifeng, Fan Shaohua, Mao Zhen, Wang Yong-Jian, Ma Daifu

机构信息

Key Laboratory for Biotechnology on Medicinal Plants of Province, School of Life Science, Xuzhou Normal University, Xuzhou 221116, China.

出版信息

J Biomed Biotechnol. 2009;2009:564737. doi: 10.1155/2009/564737. Epub 2009 Oct 26.

DOI:10.1155/2009/564737
PMID:19865488
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2766785/
Abstract

Purple sweet potato color (PSPC), a naturally occurring anthocyanin, has a powerful antioxidant activity in vitro and in vivo. This study explores whether PSPC has the neuroprotective effect on the aging mouse brain induced by D-galactose (D-gal). The mice administrated with PSPC (100 mg/kg.day, 4 weeks, from 9th week) via oral gavage showed significantly improved behavior performance in the open field and passive avoidance test compared with D-gal-treated mice (500 mg/kg.day, 8 weeks). We further investigate the mechanism involved in neuroprotective effects of PSPC on mouse brain. Interestingly, we found, PSPC decreased the expression level of glial fibrillary acidic protein (GFAP), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2), inhibited nuclear translocation of nuclear factor-kappaB (NF-kappaB), increased the activity of copper/zinc superoxide dismutase (Cu/Zn-SOD) and catalase (CAT), and reduced the content of malondialdehyde (MDA), respectively. Our data suggested that PSPC attenuated D-gal-induced cognitive impairment partly via enhancing the antioxidant and anti-inflammatory capacity.

摘要

紫甘薯色素(PSPC)是一种天然存在的花青素,在体外和体内均具有强大的抗氧化活性。本研究探讨PSPC对D-半乳糖(D-gal)诱导的衰老小鼠大脑是否具有神经保护作用。与D-gal处理组小鼠(500 mg/kg·天,8周)相比,经口灌胃给予PSPC(100 mg/kg·天,4周,从第9周开始)的小鼠在旷场试验和被动回避试验中的行为表现显著改善。我们进一步研究了PSPC对小鼠大脑神经保护作用的机制。有趣的是,我们发现,PSPC分别降低了胶质纤维酸性蛋白(GFAP)、诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的表达水平,抑制了核因子-κB(NF-κB)的核转位,提高了铜/锌超氧化物歧化酶(Cu/Zn-SOD)和过氧化氢酶(CAT)的活性,并降低了丙二醛(MDA)的含量。我们的数据表明,PSPC部分通过增强抗氧化和抗炎能力减轻了D-gal诱导的认知障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/29674b25ba3f/JBB2009-564737.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/ea0b98fb8dd1/JBB2009-564737.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/7e42cea17298/JBB2009-564737.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/4769e7b2c76e/JBB2009-564737.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/29674b25ba3f/JBB2009-564737.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/ea0b98fb8dd1/JBB2009-564737.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/7e42cea17298/JBB2009-564737.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/4769e7b2c76e/JBB2009-564737.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/f992c7256e25/JBB2009-564737.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/40e8da736e9e/JBB2009-564737.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/980c/2766785/29674b25ba3f/JBB2009-564737.006.jpg

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