• XiaoMeng Xu, XiaoHong Xu, JinLiang Cao, and LuoYang Ruan.
• Guangzhou Hospital of Integrated Traditional and West Medicine, Department of Anesthesiology, Guangzhou City, Guangdong Province, China.
• Clinics (Sao Paulo). 2024 Jan 1; 79: 100354100354.

AimThe study was to clarify the mechanism of miR-1258 targeting Prep1 (pKnox1) to control Transforming Growth Factor β1 (TGF-β1)/SMAD3 pathway in septic Acute Lung Injury (ALI)-induced oxidative stress and inflammation.MethodsBEAS-2B cells and C57BL/6 mice were used to make in vitro and in vivo septic ALI models, respectively. miR-1258 expression was checked by RT-qPCR. After transfection in the in vitro experimental model, inflammation, oxidative stress, viability, and apoptosis were observed through ELISA, MTT, and flow cytometry.ResultsIn the in vivo model after miR-1258 overexpression treatment, inflammation, oxidative stress, and lung injury were further investigated. The targeting relationship between miR-1258 and Pknox1 was tested. Low miR-1258 was expressed in septic ALI patients, LPS-treated BEAS-2B cells, and mice. Upregulated miR-1258 prevented inflammation, oxidative stress, and apoptosis but enhanced the viability of LPS-treated BEAS-2B cells. The impact of upregulated miR-1258 on LPS-treated BEAS-2B cells was mitigated by inhibiting Pknox1 expression. MiR-1258 overexpression had the alleviating effects on inflammation, oxidative stress, and lung injury of LPS-injured mice through suppressing Pknox1 expression and TGF-β1/SMAD3 cascade activation.ConclusionsThe study concludes that miR-1258 suppresses oxidative stress and inflammation in septic ALI through the Pknox1-regulated TGF-β1/SMAD3 cascade.Copyright © 2024 HCFMUSP. Published by Elsevier España, S.L.U. All rights reserved.

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