AKR1C1 alleviates LPS‑induced ALI in mice by activating the JAK2/STAT3 signaling pathway

作者：Xianjun Wang, Baocheng Yang, Yuyu Li, Jiye Luo, Yanli Wang · 发表于：Molecular Medicine Reports · 年份：2021 · DOI：10.3892/mmr.2021.12473 · 被引用次数：14 · 研究领域：Aldose Reductase and Taurine、Heme Oxygenase-1 and Carbon Monoxide、Spinal Cord Injury Research

Acute lung injury (ALI) is a respiratory tract disease characterized by increased alveolar/capillary permeability, lung inflammation and structural damage to lung tissues, which can progress and transform into acute respiratory distress syndrome (ARDS). Although there are several treatment strategies available to manage this condition, there is still no specific cure for ALI. Aldo‑keto reductase family 1 member C1 (AKR1C1) is a member of the aldo‑keto reductase superfamily, and is a well‑known Nrf2 target gene and an oxidative stress gene. The aim of the present study was to investigate the effects of AKR1C1 on a lipopolysaccharide (LPS)‑induced ALI model. After mice received LPS treatment, the mRNA expression levels of AKR1C1 in the bronchoalveolar lavage fluid and serum were measured using reverse transcription‑quantitative PCR and its relationship with the inflammatory factors and malondialdehyde levels were determined using correlation analysis. Next, AKR1C1 was overexpressed or knocked out in mice, and subsequently ALI was induced in mice using LPS. The severity of ALI, oxidative stress and inflammation in the lungs were measured, and the potential involvement of the Janus kinase 2 (JAK2)/signal transduction activator of transcription 3 (STAT3) signaling pathway was assessed by measuring the changes of lung injury parameters after the agonists of JAK2/STAT3 pathway, including interleukin (IL)‑6 and colivelin, were administrated to mice. The results revealed that AKR1C1 e...