Momordica charantia polysaccharide ameliorates D-galactose-induced aging through the Nrf2/β-Catenin signaling pathway

被引:14
|
作者
Yue, Jun [1 ,2 ]
Guo, Peng [1 ,2 ,3 ]
Jin, Yuexinzi [4 ]
Li, Ming [1 ,2 ]
Hu, Xiaotong [1 ,2 ,5 ]
Wang, Wan [6 ]
Wei, Xuewen [7 ]
Qi, Suhua [1 ,2 ,6 ]
机构
[1] Xuzhou Med Univ, Res Ctr Biochem & Mol Biol, Xuzhou, Jiangsu, Peoples R China
[2] Xuzhou Med Univ, Jiangsu Key Lab Brain Dis Bioinformat, Xuzhou, Jiangsu, Peoples R China
[3] Jinhu Cty Peoples Hosp, Dept Lab Med, Huaian 211600, Peoples R China
[4] Nanjing Med Univ, Dept Lab Med, Affiliated Hosp 1, Nanjing 210029, Peoples R China
[5] Natl Expt Teaching & Demonstrat Ctr Basic Med, Xuzhou 221004, Jiangsu, Peoples R China
[6] Xuzhou Med Univ, Med & Technol Sch, Xuzhou Key Lab Lab Diagnost, Xuzhou 221004, Jiangsu, Peoples R China
[7] Xuzhou First Peoples Hosp, Dept Lab Med, Xuzhou 221000, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Momordica charantia polysaccharide; Aging; Oxidative stress; Nrf2; beta-Catenin; OXIDATIVE STRESS; CEREBRAL ISCHEMIA/REPERFUSION; INJURY; GENETICS; GENOMICS;
D O I
10.1007/s11011-022-01103-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aging is widely thought to be associated with oxidative stress. Momordica charantia (MC) is a classic vegetable and traditional herbal medicine widely consumed in Asia, and M. charantia polysaccharide (MCP) is the main bioactive ingredient of MC. We previously reported an antioxidative and neuroprotective effect of MCP in models of cerebral ischemia/reperfusion and hemorrhage injury. However, the role played by MCP in neurodegenerative diseases, especially during aging, remains unknown. In this study, we investigated the protective effect of MCP against oxidative stress and brain damage in a D-galactose-induced aging model (DGAM). The Morris water maze test was performed to evaluate the spatial memory function of model rats. The levels of malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) were measured and telomerase activity was determined. The results showed that MCP treatment attenuated spatial memory dysfunction induced by D-galactose. In addition, MCP increased antioxidant capacity by decreasing MDA and increasing SOD and GSH levels. MCP treatment also improved telomerase activity in aging rats. Mechanistically, MCP promoted the entry of both Nrf2 and beta-Catenin into the nucleus, which is the hallmark of antioxidation signaling pathway activation. This study highlights a role played by MCP in ameliorating aging-induced oxidative stress injury and reversing the decline in learning and memory capacity. Our work provides evidence that MCP administration might be a potential antiaging strategy.
引用
收藏
页码:1067 / 1077
页数:11
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