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Glycogen synthase kinase‑3β inhibitor reduces LPS‑induced acute lung injury in mice.

Research paper by Qi Q Ding, Gaoqin G Liu, Yuanyuan Y Zeng, Jianjie J Zhu, Zeyi Z Liu, Junhong J Jiang, Jianan J Huang

Indexed on: 14 Sep '17Published on: 14 Sep '17Published in: Molecular medicine reports



Abstract

The aim of the present study was to examine the role of Wnt signaling in lipopolysaccharide (LPS)‑induced acute respiratory distress syndrome (ARDS). ARDS was induced by LPS and compared in mice treated with either glycogen synthase kinase‑3β inhibitor (GSKI) or PBS. The protein expression levels of interleukin (IL)‑6, IL‑8, tumor necrosis factor (TNF)‑α, IL‑17, IL‑18 and IL‑1β in the bronchoalveolar lavage fluid (BALF) were examined using murine cytokine‑specific enzyme‑linked immunosorbent assays. The accumulation of neutrophils and macrophages in the BALF were detected using flow cytometry. The extent of pathological lesions was evaluated using an immunohistochemical assay. The differentiation of mesenchymal stem cells (MSCs) into type II alveolar (ATII) epithelial cells was analyzed using immunofluorescence staining. Treatment with GSKI led to maintained body weights and survival in mice with LPS‑induced ARDS. Treatment with GSKI effectively reduced the levels of total protein, albumin, IgM and keratinocyte growth factor in the BALF. Smith scores showed that GSKI significantly alleviated LPS‑induced lung injury. GSKI also functioned to reduce inflammatory cell accumulation and pro‑inflammatory cytokine secretion. Finally, it was found that GSKI promoted the differentiation of MSCs into ATII epithelial cells in vivo. Taken together, the GSKI‑treated mice exhibited reduced acute lung injury through inhibited intra‑fluid inflammatory cell infiltration and decreased expression of pro‑inflammatory cytokines, and GSKI increased the differentiation of MSCs into ATII epithelial cells.