富硒木耳水提物通过抑制 RAGE/MAPK/NF-κB 通路减轻 D-半乳糖诱导的认知功能障碍、氧化应激和神经炎症。
Aqueous extracts of se-enriched Auricularia auricular attenuates D-galactose-induced cognitive deficits, oxidative stress and neuroinflammation via suppressing RAGE/MAPK/NF-κB pathway.
机构信息
Institute of Agricultural Quality Standards and Testing Technology, Jilin Academy of Agricultural Sciences, Changchun, 130033, China.
Changchun University of Chinese Medicine, Changchun, 130117, China.
出版信息
Neurosci Lett. 2019 Jun 21;704:106-111. doi: 10.1016/j.neulet.2019.04.002. Epub 2019 Apr 3.
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.
衰老是一个自然的过程，伴随着生物体认知能力下降和功能衰退。硒（Se）是一种必需的微量元素，具有抗氧化和抗炎作用。在这里，我们的研究旨在研究富硒银耳（AESAA）水提物对 D-半乳糖（D-gal）诱导衰老小鼠的保护作用，并探讨其潜在机制。通过皮下注射 D-gal（100mg/kg）12 周建立衰老小鼠模型。Morris 水迷宫（MWM）测试用于评估小鼠的认知缺陷。测量海马中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）活性和丙二醛（MDA）水平，以评估氧化应激。通过 ELISA 法测定海马中促炎细胞因子肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）的含量。进一步通过 Western blot 检测海马中 RAGE、p-Erk、p-JNK、p-P38 和 p-NF-κB 的水平，并通过免疫组化法验证 RAGE 的表达。我们发现 AESAA 补充剂显著降低了 D-gal 诱导的认知缺陷，MWM 测试结果表明小鼠的表现更好。此外，AESAA 治疗减轻了氧化应激和海马中促炎细胞因子的含量。重要的是，AESAA 抑制了 D-gal 处理小鼠海马中 RAGE、p-Erk、p-JNK、p-P38 的上调。此外，结果还表明 AESAA 抑制了 p-NF-κB 和 p-IκBα的表达。综上所述，我们的研究结果表明，AESAA 通过 RAGE/MAPK/NF-κB 信号通路有效降低了小鼠的认知障碍，减轻了氧化损伤和神经炎症，为延缓衰老过程提供了一种潜在的治疗方法。
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