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Aqueous extracts of se-enriched Auricularia auricular attenuates D-galactose-induced cognitive deficits, oxidative stress and neuroinflammation via suppressing RAGE/MAPK/NF-kappa B pathway

文献类型： 外文期刊

作者： Wang, Jingjing 1 ; Zhang, Tianzhu 2 ; Liu, Xiaoxiao 1 ; Fan, Huimei 1 ; Wei, Chunyan 1 ;

作者机构： 1.Jilin Acad Agr Sci, Inst Agr Qual Stand & Testing Technol, Changchun 130033, Jilin, Peoples R China

2.Changchun Univ Chinese Med, Changchun 130117, Jilin, Peoples R China

关键词： Se-enriched Auricularia auricular; Aqueous extracts; Cognitive deficits; Oxidative stress; Neuroinflammation; RAGE/MAPK/NF-kappa B

期刊名称：NEUROSCIENCE LETTERS （ 影响因子：3.046； 五年影响因子：2.855 ）

ISSN： 0304-3940

年卷期： 2019 年 704 卷

页码：

收录情况： SCI

摘要： Aging is a natural process that accompanied with progressive cognitive deficits and functional decline in organisms. Selenium (Se), an essential trace element, exhibits antioxidative and anti-inflammatory abilities. Here, our study aimed to investigate the protective effects of aqueous extracts of Se-enriched Auricularia auricular (AESAA) on aging mice induced by D-galactose (D-gal) and explore its potential mechanism. D-gal was administered (100 mg/kg) subcutaneously for 12 weeks to establish an aging mouse model. Morris water maze (MWM) test was conducted to assess the cognitive deficits of mice. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) activities and malondialdehyde (MDA) level in hippocampus were measured to evaluate oxidative stress. The contents of pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) in hippocampus were determined by ELISA method. Further, hippocampal levels of RAGE, p-Erk, p-JNK, p-P38 and p-NF-kappa B were detected by western blot and the RAGE expression was confirmed by immunohistochemistry. We found that AESAA supplementation significantly decreased D-gal-induced cognitive deficits, as evidenced by better performance in the MWM test. Furthermore, AESAA treatment attenuated oxidative stress and decreased the contents of pro-inflammatory cytokines in hippocampus. Importantly, AESAA inhibited the up-regulation of RAGE, p-Erk, p-JNK, p-P38 in the hippocampus of D-gal treated mice. Moreover, the results also indicated that AESAA inhibited p-NF-kappa B and p-l kappa B alpha expression. In conclusion, our findings suggest that AESAA effectively decreases cognitive impairment, alleviates oxidative damage and neuroinflammation in mice through s ItAGE/MAPK/NF-kappa B signaling pathway, which provides a potential therapy for delaying the aging process.

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