Moss Extracts as Natural Neuroprotective Agents: Mitigating LPS-Induced Neuroinflammation and Microglial Activation.

苔藓提取物作为天然神经保护剂:减轻LPS诱导的神经炎症和小胶质细胞活化

阅读:8
作者:Stojanović Tijana D, Rakić Marija R, Ćosić Marija V, Oalđe Pavlović Mariana M, Sabovljević Aneta D, Sabovljević Marko S, Božić Bojan Đ, Božić Nedeljković Biljana Đ, Vujičić Milorad M, Lunić Tanja M
Neuroinflammation plays a central role in the pathogenesis of neurodegenerative diseases, and there is increasing interest in identifying natural compounds with anti-neuroinflammatory and neuroprotective effects. In this study, we aimed to investigate the biological activities of ethanol and ethyl acetate extracts from five moss species (Dicranum scoparium, Fontinalis antipyretica, Hypnum cupressiforme, Polytrichum formosum, and Tortella tortuosa) with a focus on their neuroprotective and anti-neuroinflammatory potential. Phytochemical profiling revealed the presence of phenols (up to 24.77 mg GAE/g), phenolic acids (up to 235.48 mg CAE/g), and triterpenoids (up to 367.98 mg UAE/g). A series of in vitro assays, including acetylcholinesterase (AChE) and tyrosinase inhibition, MTT, NBT, Griess, and ELISA, were used to assess their bioactivity. Several extracts, particularly ethanolic, significantly inhibited AChE activity, while tyrosinase inhibition was moderate and concentration-dependent. Most extracts maintained >85% cell metabolic activity in BV2 mouse microglia and L929 mouse fibroblasts. Moss extracts significantly suppressed lipopolysaccharide (LPS)-induced production of reactive oxygen species (ROS), nitric oxide (NO), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) in BV2 cells and reduced microglia-mediated neurotoxicity in undifferentiated SH-SY5Y cells. These findings indicate that moss-derived extracts possess promising anti-neuroinflammatory and neuroprotective properties that warrant further investigation.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。