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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-κB pathway.
- Source :
-
Neuroscience Letters . Jun2019, Vol. 704, p106-111. 6p. - Publication Year :
- 2019
-
Abstract
- • AESAA significantly reduces cognitive impairment in d -gal-induced aging mice. • AESAA alleviates oxidative damage in d -gal-induced aging mice. • AESAA suppresses d -gal-induced neuroinflammation by decreasing pro-inflammatory cytokines. • AESAA takes effects may through inhibiting RAGE/MAPK/NF-KB signaling pathway. 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-α), interleukin-1 beta (IL-1β) 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-κB 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-κB and p-IκBα expression. In conclusion, our findings suggest that AESAA effectively decreases cognitive impairment, alleviates oxidative damage and neuroinflammation in mice through s RAGE/MAPK/NF-κB signaling pathway, which provides a potential therapy for delaying the aging process. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 03043940
- Volume :
- 704
- Database :
- Academic Search Index
- Journal :
- Neuroscience Letters
- Publication Type :
- Academic Journal
- Accession number :
- 137339982
- Full Text :
- https://doi.org/10.1016/j.neulet.2019.04.002