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茶油可缓解氯化铝处理大鼠阿尔茨海默病的进展。

Camellia oil alleviates the progression of Alzheimer's disease in aluminum chloride-treated rats.

机构信息

Department of Food Science and Biotechnology, National Chung Hsing University, 145 Xingda Road, Taichung, 40227, Taiwan.

Department of Food Science and Biotechnology, National Chung Hsing University, 145 Xingda Road, Taichung, 40227, Taiwan.

出版信息

Free Radic Biol Med. 2020 May 20;152:411-421. doi: 10.1016/j.freeradbiomed.2020.04.004. Epub 2020 Apr 12.

Abstract

Alzheimer's disease (AD), the most common type of dementia, is associated with oxidative stress, inflammation, and gut microbiota (GM) imbalance. Recent studies have demonstrated that camellia oil has antioxidant and anti-inflammatory activity and modulates the immune system and GM. However, the effect of camellia oil in alleviating AD pathogenesis remains unclear. An SD rat model of cognitive decline was established by the daily oral administration of aluminum chloride. The results revealed that the aluminum chloride-treated group exhibited deteriorated memory capacity and increased expression of AD-related proteins, whereas these features were mitigated in camellia oil-treated groups. Treatment with camellia oil increased antioxidant enzyme levels and decreased MDA levels. Additionally, camellia oil modulated the expression of cytokines by inhibiting RAGE/NF-κB signaling and microglial activation. Interestingly, autophagy-related proteins were increased in the camellia oil-treated groups. Moreover, camellia oil increased the abundance of probiotics in the GM. Camellia oil can reverse AD brain pathology by alleviating deficits in memory, increasing learning capacity, increasing antioxidant activity, modulating the expression of immune-related cytokines, enhancing autophagy and improving the composition of GM in aluminum chloride-treated rats, implying that AD pathogenesis may be mitigated by treatment with camellia oil through the microbiome-gut-brain axis.

摘要

阿尔茨海默病(AD)是最常见的痴呆症类型,与氧化应激、炎症和肠道微生物群(GM)失衡有关。最近的研究表明,油茶籽油具有抗氧化和抗炎活性,并调节免疫系统和 GM。然而,油茶籽油缓解 AD 发病机制的作用尚不清楚。通过每日口服氯化铝建立 SD 大鼠认知能力下降模型。结果表明,铝处理组表现出记忆能力恶化和 AD 相关蛋白表达增加,而油茶籽油处理组则减轻了这些特征。油茶籽油治疗可提高抗氧化酶水平并降低 MDA 水平。此外,油茶籽油通过抑制 RAGE/NF-κB 信号通路和小胶质细胞激活来调节细胞因子的表达。有趣的是,自噬相关蛋白在油茶籽油处理组中增加。此外,油茶籽油增加了 GM 中益生菌的丰度。油茶籽油通过减轻记忆缺陷、提高学习能力、提高抗氧化活性、调节免疫相关细胞因子的表达、增强自噬和改善铝处理大鼠 GM 的组成,可逆转 AD 脑病理学,这表明 AD 发病机制可能通过微生物群-肠-脑轴的作用而减轻。

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