Fig. 2: IL11 drives NASH phenotypes through autocrine effects in lipotoxic hepatocytes and paracrine activity in hepatic stellate cells.

a–l Data for palmitate (0.5 mM) loading experiment on primary human hepatocytes (24 h) in the presence of either IgG (2 µg/ml), anti-IL11RA (X209, 2 µg/ml), or sgp130 (1 µg/ml). a IL11, b IL6, c CCL2, and d CCL5 protein secretion levels as measured by ELISA of supernatants (n = 3). e Representative FSC plots and f quantification of PI^+ve hepatocytes stimulated with palmitate (n = 3). g ALT levels in supernatants (n = 3). h Total and reduced hepatocyte glutathione (GSH) levels (n = 4). i Representative fluorescence images of DCFDA (2′,7′-dichlorofluorescein diacetate) staining for ROS detection (scale bars, 100 µm) (n = 4 independent experiments). j Western blots of phospho-ERK, ERK, phospho-JNK, JNK, cleaved caspase-3, caspase-3, NOX4, and GAPDH. Data from two independent biological experiments are shown. k Percentage of fatty acid oxidation by Seahorse assay (n = 10). l Representative fluorescence images (scale bars, 100 µm) of ACTA2^+ve cells and Collagen I immunostaining for experiment shown in Supplementary Fig. 5j (n = 2 independent experiments, 14 measurements per condition per experiment). a–d, f, g Mean ± SD; h, k data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box), and min–max values (whiskers). a–d, f–h, k One-way ANOVA with Tukey’s correction. Source data are provided as a Source data file.