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Fig. 1 | Respiratory Research

Fig. 1

From: Vildagliptin ameliorates pulmonary fibrosis in lipopolysaccharide-induced lung injury by inhibiting endothelial-to-mesenchymal transition

Fig. 1

Vildagliptin restored normal pulmonary structure in a mouse model of post-ALI pulmonary fibrosis.

a Flow cytometry (FCM) analyses revealed that the number of CD26-expressing pulmonary vascular endothelial cells (PVECs: CD31+/CD45− cells) isolated from mice was significantly increased 14 days after LPS administration. This effect was significantly inhibited by systemic vildagliptin administration (*P < 0.05, N = 5). b Representative FCM panels with CD26+-gated PVECs. c Immunohistochemistry also revealed that the number of CD26-expressing pulmonary vascular endothelial cells (PVECs: CD31+CD45− cells) significantly increased 14 days after LPS administration, and this increase could be significantly inhibited by systemic vildagliptin administration. CD31, green; CD26, blue; CD45, red. Scale bars, 100 μm. d Effect of bleomycin on lung architecture in vehicle- or vildagliptin-treated mice as shown by Masson’s trichrome staining of lung tissue sections 28 days after LPS administration. e The Ashcroft fibrosis score was used to compare the degrees of pulmonary fibrosis. Pulmonary fibrosis induced by LPS was significantly attenuated by vildagliptin treatment (*P < 0.05, N = 5). Scale bars, 100 μm.

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