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3,6'-Disinapoylsucrose alleviates the amyloid precursor protein and lipopolysaccharide induced cognitive dysfunction through upregulation of the TrkB/BDNF pathway
Journal of Asian Natural Products Research ( IF 1.3 ) Pub Date : 2022-06-07 , DOI: 10.1080/10286020.2022.2069565
Yun-Ting Wang 1, 2 , Han Wang 2 , Wu-Jiang Ren 2 , Xue-Ling Dai 1 , Qing Huo 2 , Shuo Wang 3 , Ya-Xuan Sun 1
Affiliation  

Abstract

The aim of this study is to explore the effect and mechanism of 3,6’-disinapoylsucrose (DISS) on an Alzheimer's disease (AD) mice model induced by APPswe695 lentivirus (LV) and intraperitoneal injection of lipopolysaccharide (LPS). The results show that DISS improves cognitive ability, decreases the levels of IL-2, IL-6, IL-1β, and TNF-α, reduces the expression of NF-κB p65, and alleviates Aβ deposition and nerve cell damage. DISS can regulate tyrosine kinase B (TrkB)/brain-derived neurotrophic factor (BDNF) signaling in the hippocampus. In summary, DISS can significantly alleviate neuroinflammation, spatial learning and memory disorders in AD model mice.



中文翻译:

3,6'-Disinapoylsucrose 通过上调 TrkB/BDNF 通路减轻淀粉样前体蛋白和脂多糖诱导的认知功能障碍

摘要

本研究旨在探讨3,6'-二萘酚蔗糖(DISS)对APPswe695慢病毒(LV)腹腔注射脂多糖(LPS)诱导的阿尔茨海默病(AD)小鼠模型的影响及机制。结果表明,DISS提高认知能力,降低IL-2、IL-6、IL-1β和TNF-α水平,降低NF-κB p65的表达,减轻Aβ沉积和神经细胞损伤。DISS 可以调节海马体中的酪氨酸激酶 B (TrkB)/脑源性神经营养因子 (BDNF) 信号。综上所述,DISS可显着缓解AD模型小鼠的神经炎症、空间学习记忆障碍。

更新日期:2022-06-07
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