Fig. 3: HSC-specific FGF18 deficiency aggravates liver apoptosis and the inflammatory response during hepatic IRI. | Nature Communications

Fig. 3: HSC-specific FGF18 deficiency aggravates liver apoptosis and the inflammatory response during hepatic IRI.

From: FGF18 alleviates hepatic ischemia-reperfusion injury via the USP16-mediated KEAP1/Nrf2 signaling pathway in male mice

Fig. 3: HSC-specific FGF18 deficiency aggravates liver apoptosis and the inflammatory response during hepatic IRI.The alternative text for this image may have been generated using AI.

Fgf18△HSC mice were constructed by using Fgf18f/f and GFAP-specific Cre mice. A Schematic diagram of mouse breeding. And the genotype of Fgf18△HSC mice and the knockdown efficiency of FGF18 were verified by RT-PCR (n = 3). (Scheme is Created with BioRender.com). B Serum ALT and AST level (n = 5). C H&E staining of liver sections (n = 5). Scale bar = 100 μm. D–F TUNEL staining, c-CAS-3 immunohistochemistry, and MPO staining of liver sections (n = 5). Scale bar=100 μm. G Relative protein expression by western blotting (n = 3). H RNA-seq analysis of livers from Fgf18f/f mice and Fgf18△HSC mice subjected to I/R (1 h/6 h). Red indicated upregulation while blue indicated downregulation (n = 3). The statistical significance of differences were assessed by two-tailed student unpaired t-test for (C–F). Other assays were assessed by one-way ANOVA, followed by Tukey’s multiple comparison test. Data are presented as means ± SEM with individual values. All numbers (n) are biologically independent experiments. Source data are provided as a Source Data file.

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