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Vitamin D exerts neuroprotection via SIRT1/nrf-2/ NF-kB signaling pathways against D-galactose-induced memory impairment in adult mice
Neurochemistry international ( IF 4.2 ) Pub Date : 2020-11-04 , DOI: 10.1016/j.neuint.2020.104893
Ammar Ali 1 , Shahid Ali Shah 2 , Nasib Zaman 3 , Muhammad Nazir Uddin 3 , Wajid Khan 3 , Abid Ali 4 , Muhammad Riaz 5 , Atif Kamil 1
Affiliation  

Vitamin D (Vt. D) is one of the vital hormone having multiple functions in various tissues, including brain. Several evidences reported that Vt. D plays a significant part in memory and cognition as its inadequate amount may accelerate cognitive impairment. This study shows for the first time the antioxidant potential of Vt. D against D-Galactose (D-gal) induced oxidative stress mediated Alzheimer disease (AD) pathology in male adult albino mice. The result reveals that the mice exposed to D-gal (120 mg/kg) for eight weeks have pre-and post-synaptic dysfunction and impaired memory investigated through Morris water maze and Y-maze tests. This is followed by the suppressed Nuclear factor erythroid 2-related factor 2 (NRF2), Heme Oxygenase-1 (HO-1) and elevated expressions of Nuclear Factor kappa B (NF-kB), Tumor Necrosis Factor alpha (TNF-α) and Interleukin 1 beta (IL-1β) proteins in the brain homogenates evaluated through western blotting technique. On the other hand Vt. D (100 μg/kg) administration (three times a week for 4 weeks) activated Silent mating type information regulation 2 homolog 1 (SIRT1) and significantly improved both the neuronal synapse and memory, reduced oxidative stress by upregulating NRF-2 and HO-1 and downregulating NF-kB, TNF-α and IL-1β proteins expression. Most importantly, Vt. D significantly abrogate the amyloidogenic pathway of amyloid beta (Aβ) production against D-gal in the brains of adult male albino mice. These results reveal that Vt. D being an antioxidant agent plays a vital role in reducing the AD pathophysiology in D-gal induced animal model of aging, therefore act as a potential drug candidate in neurodegenerative diseases.



中文翻译:

维生素 D 通过 SIRT1/nrf-2/NF-kB 信号通路发挥神经保护作用,对抗 D-半乳糖诱导的成年小鼠记忆障碍

维生素 D (Vt. D) 是一种重要的激素,在包括大脑在内的各种组织中具有多种功能。一些证据表明,Vt. D 在记忆和认知方面起着重要作用,因为其数量不足可能会加速认知障碍。这项研究首次显示了 Vt. D 对 D-半乳糖 (D-gal) 诱导的氧化应激介导的成年雄性白化小鼠阿尔茨海默病 (AD) 病理的抗氧化潜力。结果表明,暴露于 D-gal (120 mg/kg) 八周的小鼠具有突触前和突触后功能障碍以及通过莫里斯水迷宫和 Y 迷宫测试调查的记忆力受损。其次是抑制的核因子红细胞 2 相关因子 2 (NRF2)、血红素加氧酶-1 (HO-1) 和核因子 kappa B (NF-kB) 的表达升高,通过蛋白质印迹技术评估脑匀浆中的肿瘤坏死因子 α (TNF-α) 和白细胞介素 1 β (IL-1β) 蛋白。另一方面,Vt. D (100 μg/kg) 给药(每周 3 次,持续 4 周)激活沉默交配型信息调节 2 同源物 1 (SIRT1) 并显着改善神经元突触和记忆,通过上调减少氧化应激NRF-2 和 HO-1 以及下调 NF-kB、TNF-α 和 IL-1β 蛋白的表达。最重要的是,Vt. D 显着消除了成年雄性白化小鼠大脑中针对 D-gal 产生淀粉样蛋白 β (Aβ) 的淀粉样蛋白生成途径。这些结果表明,作为一种抗氧化剂的 Vt. D 在减少 D-gal 诱导的衰老动物模型中的 AD 病理生理方面起着至关重要的作用,

更新日期:2020-11-21
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