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YBX-1 减轻脓毒症刺激的肺上皮细胞损伤。

YBX-1 alleviates sepsis-stimulated lung epithelial cell injury.

机构信息

Department of Emergency Medicine, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.

Department of Emergency Medicine, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China;

出版信息

Allergol Immunopathol (Madr). 2024 Mar 1;52(2):60-67. doi: 10.15586/aei.v52i2.1068. eCollection 2024.

DOI:10.15586/aei.v52i2.1068
PMID:38459892
Abstract

OBJECTIVE

To explore the role of Y-box binding protein 1 (YBX-1) in the lipopolysaccharide (LPS)-stimulated inflammation and oxidative stress of BEAS-2B cell line and clarify the underlying mechanism.

METHODS

LPS-stimulated BEAS-2B cells were used as a cell model of sepsis-stimulated acute lung injury (ALI). Immunoblot and quantitative polymerase chain reaction assays were used to detect the expression of YBX-1 in LPS-stimulated BEAS-2B cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide, TdT-mediated dUTP nick end labeling, and immunoblot assays were conducted to determine the effects of YBX-1 on cell survival. JC-1 staining and adenosine triphosphate production were used to detect the effects of YBX-1 on mitochondrial function. Immunostaining and enzyme-linked immunosorbent serologic assay were performed to examine the effects of YBX-1 on the inflammation and oxidative stress of cells. Immunoblot assay was conducted to confirm the mechanism.

RESULTS

YBX-1 was lowly expressed in LPS-stimulated BEAS-2B cells and enhanced the survival of LPS-stimulated lung epithelial cells. In addition, YBX-1 improved mitochondrial function of LPS-stimulated BEAS-2B cells. YBX-1 inhibited the inflammation and oxidative stress of LPS-stimulated BEAS-2B cells. Mechanically, YBX-1 inhibited mitogen-activated protein kinase (MAPK) axis, thereby alleviating sepsis-stimulated ALI.

CONCLUSION

YBX-1 alleviated inflammation and oxidative stress of LPS-stimulated BEAS-2B cells via MAPK axis.

摘要

目的

探讨 Y 盒结合蛋白 1(YBX-1)在脂多糖(LPS)刺激的 BEAS-2B 细胞系炎症和氧化应激中的作用,并阐明其潜在机制。

方法

采用 LPS 刺激的 BEAS-2B 细胞作为脓毒症刺激的急性肺损伤(ALI)的细胞模型。采用免疫印迹和定量聚合酶链反应检测 LPS 刺激的 BEAS-2B 细胞中 YBX-1 的表达。采用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基-2H-四唑溴盐(MTT)、末端转移酶介导的 dUTP 缺口末端标记(TUNEL)和免疫印迹检测 YBX-1 对细胞存活的影响。JC-1 染色和三磷酸腺苷(ATP)产生用于检测 YBX-1 对线粒体功能的影响。免疫染色和酶联免疫吸附试验(ELISA)用于检测 YBX-1 对细胞炎症和氧化应激的影响。免疫印迹用于验证机制。

结果

YBX-1 在 LPS 刺激的 BEAS-2B 细胞中低表达,并增强 LPS 刺激的肺上皮细胞的存活。此外,YBX-1 改善了 LPS 刺激的 BEAS-2B 细胞的线粒体功能。YBX-1 抑制了 LPS 刺激的 BEAS-2B 细胞的炎症和氧化应激。机制上,YBX-1 抑制丝裂原活化蛋白激酶(MAPK)轴,从而减轻脓毒症引起的 ALI。

结论

YBX-1 通过 MAPK 轴缓解 LPS 刺激的 BEAS-2B 细胞的炎症和氧化应激。

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