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.