Fig. 7: Pharmacological Ire1α inhibition reduces ischemic kidney damage.

Quantification of (A) blood urea nitrogen (BUN) and (B) creatinine levels in mice treated with either vehicle, 4μ8c (20 mg/kg or 40 mg/kg), or liproxstatin-1 (10 mg/kg) then subjected to ischemia–reperfusion (IR). C Representative microscopic images of haematoxylin and eosin (H&E) staining of the renal cortex after treatment. Selected representative regions are enlarged and displayed at the corner. Dash lines outline damaged renal tubules (as characterized by tubular dilatation, tubule brush border loss, flattened epithelial cells or sloughing of cells). Scale bars: 200 μm. The histogram on the right shows the quantification of renal tubule damages. D. Representative images of lipid peroxidation marker 4-HNE immunohistochemistry staining of renal cortex after treatment. Scale bars: 200 μm. The histogram on the right shows the quantification of 4-HNE-positive tubules in the renal cortex. Data are presented as mean ± s.d. in (A, B) and the right panels of (C and D), with n = 5 (vehicle only), n = 7 (IR + vehicle), n = 4 (IR + 20 mg/kg 4μ8c), n = 7 (IR + 40 mg/kg 4μ8c) and n = 8 (IR + 10 mg/kg liproxstatin-1) independent kidneys in the corresponding groups. P values were calculated from unpaired two-tailed Student’s t test. Source data are provided as a Source Data file.