Mir-204 Regulates LPS-Induced A549 Cell Damage by Targeting FOXK2.

Shufen Li,Zhuohui Song,Gaiping Shang,Lijing Gao,Ting Li,Lifen Zhao,Xujiong Li

doi:10.1155/2021/7404671

Shufen Li, Zhuohui Song + Show 5 more

Open Access

https://doi.org/10.1155/2021/7404671

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Abstract

Objective To assess whether miR-204 and HA affect A549 cell injury induced by lipopolysaccharide. Material and Methods. 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. Results LPS can significantly inhibit the viability of A549 cells, induce cell apoptosis, and promote the release of IL-6, IL-1β, and TNF-α, 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-κB. Conclusions miR-204 participates in the protection of HA acute lung injury by targeting FOXK2.

Highlights

Acute lung injury (ALI) has a high morbidity and mortality [1,2,3]
Further ELISA testing showed that inflammatory factors in the cell supernatant of the LPS group were significantly increased, which were inhibited by Hirsutanol A (HA) (Figures 1(e) and 1(f ))
Acute lung injury caused by sepsis appears first [18]. e results of this study showed that, in the LPS-induced in vitro model of ALI, miR-204 was significantly downregulated. e downregulated miR-204 activates the NF-κB pathway by targeting FOXK2, promotes the release of inflammatory factors, and induces A549 cell apoptosis, and HA can exert ALI protection by upregulating miR-204

Summary

Introduction

Acute lung injury (ALI) has a high morbidity and mortality [1,2,3]. ALI is featured as destruction of the alveolar-capillary membrane barrier leading to inflammation and subsequent lung dysfunction [4, 5]. erefore, inhibiting inflammation may be critical to ALI treatment. Studies have found that HA can induce tumor cell apoptosis by upregulating cleaved-caspase-3, but it is rarely reported in ALI and ARDS [6, 7]. Recent studies demonstrated that [8, 9] miR-204 participates in sepsis. Recent studies have shown that [13, 14] miR-204 is a new regulator of innate immune response, which can significantly improve the survival rate of LPS-induced sepsis by preventing NF-κB-mediated inflammation. Is study established an acute lung injury model induced by lipopolysaccharide and explored the specific mechanism of miR-204 in lung injury induced by lipopolysaccharide and the specific mechanism of HA Recent studies have shown that [13, 14] miR-204 is a new regulator of innate immune response, which can significantly improve the survival rate of LPS-induced sepsis by preventing NF-κB-mediated inflammation. is study established an acute lung injury model induced by lipopolysaccharide and explored the specific mechanism of miR-204 in lung injury induced by lipopolysaccharide and the specific mechanism of HA

Methods

Results

Conclusion