Palmitic acid increasing the entry of lipopolysaccharide into microglial cytosol and eliciting pyroptosis and apoptosis
10.16098/j.issn.0529-1356.2025.04.004
- VernacularTitle:棕榈酸促进脂多糖进入小胶质细胞并引发凋亡和焦亡
- Author:
Yu-Hu FENG
1
;
Yan-Zhuo YANG
;
Hai-Yan LÜ
;
Qing-Ting YU
;
Zui-Su YANG
;
Fa-Lei YUAN
Author Information
1. 浙江海洋大学食品与药学学院药学系,浙江省海洋生物医用制品重点工程技术研究中心,浙江舟山 316000
- Keywords:
Palmitic acid;
Microglia;
Pyroptosis;
Wedelolactone;
BV-2 microglial cell;
Western blotting;
Mouse
- From:
Acta Anatomica Sinica
2025;56(4):404-412
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the types and mechanisms of microglial cell death induced by interaction between palmitic acid(PA)and lipopolysaccharide(LPS).Methods BV-2 microglial cells were divided into three groups for apoptosis research,BSA group,PA treatment group,and staurosporine(STA)group.They were further divided into four groups for necrosis research,BSA group,BSA+inhibitor group,PA group,and PA+inhibitor group.Western blotting was conducted to assess the expression levels of key proteins involved in apoptosis and necrosis pathways.The effect of PA on microglial cells was validated through feeding a high-fat diet to Institute of Cancer Research(ICR)mice.Results Apoptotic microglia were observed in both BSA group and PA group,PA significantly induced the activation of caspase-3,caspase-7,and poly ADP-ribose polymerase(PARP).However,compared to the BSA group,the level of activated Caspase-7 in the STA group did not change significantly.Inhibition of ferroptosis,necroptosis,or autophagy did not protect against PA-induced cell damage,while the Caspase-11 inhibitor,wedelolactone(WE),significantly improved PA induced cell damage.This study also found that PA could promote LPS entry into microglial cells and induce pyroptosis.This phenomenon and the protective effect of WE were further confirmed in a high-fat diet mouse model through immunofluorescent staining and Western blotting.Conclusion PA induces apoptosis and pyroptosis in microglial cells,while simultaneously promoting LPS entry into microglial cells and inducing pyroptosis.
