脂氧素A4促进自噬并抑制牙龈卟啉单胞菌脂多糖诱导的巨噬细胞炎性小体活性过度激活。
Lipoxin A4 promotes autophagy and inhibits overactivation of macrophage inflammasome activity induced by Pg LPS.
作者信息
Zhao Jie, Geng Wenjing, Wan Kefei, Guo Kailei, Xi Fengjun, Xu Xiangqun, Xiong Xiujuan, Huang Xu, Liu Jiayi, Kuang Xiaodong
机构信息
Affiliated Stomatological Hospital of Nanchang University, China.
Queen Mary College of Nanchang University, China.
出版信息
J Int Med Res. 2021 Feb;49(2):300060520981259. doi: 10.1177/0300060520981259.
OBJECTIVE
To explore the role of lipoxin A4 (LXA4) on inflammasome and inflammatory activity in macrophages activated by lipopolysaccharide (PgLPS) one of the major causative agents of chronic periodontitis.
METHODS
The mouse macrophage cell line RAW264.7 was used to produce an activated inflammation model. Markers of inflammasome and inflammatory activity and autophagy were assessed by ELISA, reverse transcription polymerase chain reaction (RT-PCR), and Western blot assay.
RESULTS
Markers of inflammasome activity, inflammation and autophagy increased with Pg LPS concentration. They also increased with increasing exposure to Pg LPS up to 12h but decreased at 24h. However, markers of autophagy increased. Phosphorylated NF-κBp65 decreased with LXA4, which was similar to results obtained with the autophagy inducer, rapamycin.
CONCLUSIONS
LXA4 promoted autophagy and inhibited activation of inflammasomes and inflammation markers in macrophage inflammation induced by PgLPS and this action was linked to the phosphorylation of NF-κB.
目的
探讨脂氧素A4（LXA4）在慢性牙周炎主要致病菌之一牙龈卟啉单胞菌脂多糖（PgLPS）激活的巨噬细胞中对炎性小体和炎症活性的作用。
方法
使用小鼠巨噬细胞系RAW264.7建立激活的炎症模型。通过酶联免疫吸附测定（ELISA）、逆转录聚合酶链反应（RT-PCR）和蛋白质免疫印迹法评估炎性小体、炎症活性和自噬的标志物。
结果
炎性小体活性、炎症和自噬的标志物随Pg LPS浓度升高而增加。它们也随Pg LPS暴露时间延长至12小时而增加，但在24小时时下降。然而，自噬标志物增加。LXA4使磷酸化的NF-κBp65减少，这与自噬诱导剂雷帕霉素的结果相似。
结论
LXA4促进自噬，并抑制PgLPS诱导的巨噬细胞炎症中炎性小体和炎症标志物的激活，且该作用与NF-κB的磷酸化有关。
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