Protective effects of ginsenoside Rg1 on neuronal senescence due to inhibition of NOX2 and NLRP1 inflammasome activation in SAMP8 mice

被引:9
|
作者
Chen, Yali [1 ]
Ding, Shixin [1 ]
Zhang, Han [1 ]
Sun, Zhenghao [1 ]
Shen, Xiaoyan [1 ]
Sun, Lingling [1 ]
Yin, Yanyan [1 ]
Qun, Sen [2 ]
Li, Weizu [1 ]
机构
[1] Anhui Med Univ, Dept Pharmacol, Basic Med Coll, Key Lab Antiinflammatory & Immunopharmacol,Minist, Hefei 230032, Peoples R China
[2] Univ Sci & Technol China, Affiliated Hosp 1, Dept Neurol, Hefei 230001, Peoples R China
基金
中国国家自然科学基金;
关键词
Ginsenoside Rg1; ROS oxidative stress; NADPH oxidase 2; NLRP1; inflammasome; SAMP8; OXIDATIVE STRESS; ALZHEIMERS-DISEASE; BRAIN; MEMORY; DEGENERATION; HIPPOCAMPUS; MECHANISMS; EXPRESSION; NEURODEGENERATION; DYSFUNCTION;
D O I
10.1016/j.jff.2019.103713
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
With aging of population, aging-related neurodegenerative diseases have become a major public health concern. Oxidative stress and neuroinflammation have been reported to play important roles in the aging process. Ginsenoside Rg1 (Rg1) is the main active ingredient in ginseng, and may be a potential agent for neurodegenerative diseases. In the present study, we investigated the effects of Rg1, tempol (ROS scavenger) and apocynin (NOX inhibitor) treatment for 9 weeks on cognitive performance, neuronal damage, and NOX2 and NLRP1 inflammasome expressions in 8-month old SAMP8 mice. The results showed that Rg1 alleviated learning and memory impairment and neuronal damage in SAMP8 mice. Meanwhile, Rg1 could reduce production of ROS and decreased expressions of NOX2 and NLRP1-related proteins in brain cortex and hippocampus tissues in SAMP8 mice. The findings suggest that Rg1 can alleviate aging-related neuronal damage, the mechanisms may be involved in reducing NOX2-mediated ROS generation and inhibiting NLRP1 inflammasome activation.
引用
收藏
页数:13
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