Investigation of the mechanisms of action of sodium butyrate in ameliorating the pathological processes in an Alzheimer's disease model
10.3760/cma.j.issn.0254-9026.2023.11.012
- VernacularTitle:丁酸钠改善阿尔茨海默病模型的病理作用机制探讨
- Author:
Jiaxi XU
1
;
Zhengming LIAO
;
Enyan YU
Author Information
1. 浙江省立同德医院精神卫生科，杭州 311122
- Keywords:
Alzheimer disease;
Inflammation;
Autophagy;
Sodium butyrate
- From:
Chinese Journal of Geriatrics
2023;42(11):1337-1342
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of sodium butyrate(NaB)on pathological processes such as autophagy and inflammation in an Alzheimer's disease(AD)model and related mechanisms.Methods:Aβ 25-35's action on PC12 cells was used to establish an in vitro AD model, in which microglial BV2 were treated with NaB.Based on treatments, there were a PC12 cells group, a PC12 cells+ Aβ 25-35 group, a PC12 cells+ Aβ 25-35+ NaB group, a BV2 cells group, a BV2 cells+ Aβ 25-35 group, and a BV2 cells+ Aβ 25-35+ NaB group.The expression of markers of the autophagy pathway and inflammatory proteins was evaluated by Western blot, immunofluorescence and EdU staining.Results:NaB was able to promote cell proliferation in the AD model and reduce the level of Tau protein hyperphosphorylation.NaB also inhibited the inflammatory response of microglia and reduce the expression of inflammatory response marker NLRP3(148.313±0.973 vs.113.291±1.218, t=38.91, P<0.001). At the same time, NaB promoted the expression of autophagy pathway proteins(including Beclin-1, LAMP-1 and LC3 Ⅱ/Ⅰ)in microglia. Conclusions:NaB can mitigate pathological changes in an AD model by promoting autophagy and reducing the inflammatory response.
