Department of Physiology, Changzhi Medical College, Changzhi, Shanxi 046000, China.
Department of Respiratory and Critical Care Medicine, Shanxi Academy of Hospital Sciences, Taiyuan, Shanxi 046000, China.
J Healthc Eng. 2021 Nov 30;2021:7404671. doi: 10.1155/2021/7404671. eCollection 2021.
To assess whether miR-204 and HA affect A549 cell injury induced by lipopolysaccharide. . A549 cells were treated with hirsutanol A, and cell damage was induced by LPS followed by analysis of cell proliferation by CCK-8, cell apoptosis by flow cytometry, apoptosis-related protein expression by western blot, downstream target of miR-20 by dual-luciferase reporter gene, and inflammatory factors by ELISA and PCR.
LPS can significantly inhibit the viability of A549 cells, induce cell apoptosis, and promote the release of IL-6, IL-1, and TNF-, while HA pretreatment can target FOXK2 by upregulating miR-204 levels, thereby alleviating apoptosis and promoting cell viability and at the same time inhibiting the release of inflammatory factors by inhibiting the activation of NF-B.
miR-204 participates in the protection of HA acute lung injury by targeting FOXK2.
评估 miR-204 和透明质酸 (HA) 是否影响脂多糖诱导的 A549 细胞损伤。用胡蔓藤碱 A 处理 A549 细胞,用 LPS 诱导细胞损伤,然后通过 CCK-8 检测细胞增殖,流式细胞术检测细胞凋亡,Western blot 检测凋亡相关蛋白表达,双荧光素酶报告基因检测 miR-204 的下游靶基因,ELISA 和 PCR 检测炎症因子。结果:LPS 可显著抑制 A549 细胞活力,诱导细胞凋亡,并促进 IL-6、IL-1 和 TNF- 的释放,而 HA 预处理可通过上调 miR-204 水平靶向 FOXK2,从而减轻细胞凋亡,促进细胞活力,同时通过抑制 NF-B 的激活抑制炎症因子的释放。结论:miR-204 通过靶向 FOXK2 参与 HA 急性肺损伤的保护。