Fig 1: FGF21 is induced after MV in patients and mice. A. The average serum FGF21 increased in patients after mechanical ventilation (N = 69); B. The average serum FGF21 increased in patients after short duration (< 4 h) of mechanical ventilation (N = 33); C. The average serum FGF21 increased in patients after long duration (> 4 h) of mechanical ventilation (N = 36); D. The elevated FGF21 level was positively correlated with duration of mechanical ventilation; E. Serum FGF21 increased in VILI mice (N = 6, 0 h referred to the time point immediately after VILI modeling); F. FGF21 protein expression in mice lung/liver tissues after mechanical ventilation; G. Serum IL-1β increased in VILI mice (N = 6); H. Serum IL-18 increased in VILI mice (N = 6); ns, no significance, *P < 0.05, **P < 0.01; MV, mechanical ventilation; VILI, ventilator-induced lung injury
Fig 2: FGF21 treatment inhibits endothelial injury and downregulates pulmonary interstitial pro-fibrosis factors. A. Immunofluorescence of vascular endothelial marker, VE-cadherin, in lung tissue; B. Immunofluorescence of pulmonary interstitial marker, α-SMA, in lung tissue; C. Immunofluorescence of pulmonary interstitial marker, vimentin, in lung tissue; N = 6 in A-C; ns, no significance, *P < 0.05, **P < 0.01 vs. Control; #P < 0.05, ##P < 0.01 vs. PBS; Bar scale = 100 μm; MV, mechanical ventilation; DAPI, 4',6-diamidino-2-phenylindole
Fig 3: FGF21 treatment alleviates VILI in mice. A. Hematoxylin–eosin staining of lung tissues and average lung injury scores analysis of lung slices (N = 5, scale bar = 500 μm in low-power images and = 50 μm in amplified images); B. TUNEL staining of lung tissues and dead cells counting of lung slices (N = 5, scale bar = 100 μm); C. H&E staining of exfoliated cells and total cell counting in BALF (N = 6, scale bar = 20 μm); D. Neutrophil count in BALF; E. The content of Evans blue dye in lung tissue; F. Protein concentration in BALF; G. Wet/dry ratio of lung tissue; H. MPO activity in lung tissue. I. Trolox-equivalent antioxidant capacity in mice lung tissue. J. ATP level in mice lung tissue; K. Timeline of the treating experiment. ns, no significance, *P < 0.05, **P < 0.01 vs. Control; #P < 0.05, ##P < 0.01 vs. PBS; MV, mechanical ventilation; TUNEL, TdT-mediated dUTP nick end labeling; DAPI, 4',6-diamidino-2-phenylindole; BALF, bronchoalveolar lavage fluid; MPO, Myeloperoxidase; TEAC, Trolox-equivalent antioxidant capacity
Fig 4: FGF21 protects against VILI via inhibiting NLRP3/Caspase-1/GSDMD pyroptotic pathway. A. Relative caspase-1 activity in mice lung tissue; B-E. Relative mRNA expression levels of key nodes in NLRP3/caspase-1/GSDMD pathway (N = 6, *P < 0.05, **P < 0.01); F–H. Relative protein expression levels of key nodes in NLRP3/caspase-1/GSDMD pathway (N = 3; ns, no significance, *P < 0.05, **P < 0.01 vs. Control; #P < 0.05, ##P < 0.01 vs. PBS). Lung tissue samples in Fig. 6 are from the same batch of mice in Fig. 3
Fig 5: FGF21 treatment ameliorates MS-induced injury in a cell model. A. FGFR1 expression in mouse liver, lung, and primary lung microvascular endothelial cells; B. Cell viability assessment by CCK8 assay (N = 6); C. Relative LDH level in cell culture supernatant (N = 6); D. Detection of reactive oxygen species by dichlorodihydrofluorescein probe in situ (N = 3, scale bar = 100 μm); E. Trolox-equivalent antioxidant capacity in cells (N = 6); F. Superoxide dismutase activity in cells (N = 6). G. Adenosine triphosphate level in cells (N = 6); H. Mitochondrial membrane potential and cell death staining (N = 6, scale bar = 100 μm); ns, no significance, *P < 0.05, **P < 0.01 vs. Control; #P < 0.05, ##P < 0.01 vs. PBS; FGFR1, fibroblast growth factor receptor 1; LMVESs, lung microvascular endothelial cells; MS, mechanical stretch; LDH, lactate dehydrogenase; DCF, dichlorodihydrofluorescein; TEAC, Trolox-equivalent antioxidant capacity; SOD, Superoxide dismutase
Supplier Page from MedChemExpress for FGF-21 Protein, Mouse