上睑下垂
棕榈油酸
碘化丙啶
小胶质细胞
细胞凋亡
程序性细胞死亡
细胞生物学
未折叠蛋白反应
内质网
化学
炎症
生物
生物化学
棕榈酸
脂肪酸
免疫学
作者
Qingting Yu,Yanzhuo Yang,Xu Ting,Yingmu Cai,Zuisu Yang,Falei Yuan
出处
期刊:PLOS ONE
[Public Library of Science]
日期:2024-01-19
卷期号:19 (1): e0297031-e0297031
标识
DOI:10.1371/journal.pone.0297031
摘要
Although palmitoleic acid (POA) is a lipokine with beneficial effects on obesity and is produced as a byproduct from the manufacture of prescription omega-3 fatty acids, its role in nervous system inflammation is still unknown. This study aims to examine the mechanisms and protective effects of POA against palmitic acid (PA)-induced microglial death. PA-induced microglial death was used as a model for POA intervention. Various inhibitors were employed to suppress potential routes of PA entry into the cell. Immunofluorescence staining and Western blotting were conducted to elucidate the protective pathways involved. The results suggest POA has the potential to eliminate PA-induced lactate dehydrogenase (LDH) release, which decreases the overall number of propidium iodide (PI)-positive cells compared with control. Moreover, POA has the potential to significantly increase lipid droplets (LDs) in the cytoplasm, without causing any lysosomal damage. POA inhibited both canonical and non-canonical gasdermin D (GSDMD)-mediated pyroptosis and gasdermin E (GSDME)-mediated pyroptosis, which PA typically induces. Additionally, POA inhibited the endoplasmic reticulum (ER) stress and apoptosis-related proteins induced by PA. Based on the findings, POA can exert a protective effect on microglial death induced by PA via pathways related to pyroptosis, apoptosis, ER stress, and LDs.
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