FIGURE 1. Aristolochic acid I (AAI) induces kidney tissue PANoptosis and damage.
(A) C57BL/6 mice aged 6–8 weeks were treated with AAI and euthanized three days after AAI treatment. (B) Creatinine (Cr) and blood urea nitrogen (BUN) were assessed three days after AAI treatment. (C) Representative hematoxylin-eosin (H&E)-stained sections of kidney from wild-type (WT) and AAI-treated mice (Scale bar = 40 μm). (D) Western blotting analyses of cleaved-caspase-3, pMLKL, and GSDMD-N in AAI-induced AKI mice. (E) Photomicrographs of immunohistochemical sections from WT and AAI-treated mice with cleaved-caspase-3, pMLKL, and GSDMD-N in both AAI-treated mice and WT mice (Scale bar = 40 μm). (F) Western blotting analyses of cleaved-caspase-3, pMLKL, and GSDMD-N in AAI-treated mTECs. (G) Immunofluorescence staining of cleaved-caspase-3, pMLKL, and GSDMD-N in AAI-treated mTECs (Scale bar = 100 μm). Data are presented as the mean ± SEM, n = 5. ns, not significant; *P < 0.05, significantly different, as indicated.