Fig. 1

CX3CL1 deficiency alleviated kidney function damage in cisplatin-induced model mice. WT mice and CX3CL1-KO mice received cisplatin injections at 48 h. A Examination of the kidney’s histology using representative images of H&E and PAS staining. B The serum levels of BUN and Scr were evaluated in all mice groups. C Western blotting was conducted to determine the relative expression patterns of podocin, CX3CL1, nephrin, and WT1. D Representative images of podocyte ultrastructure in kidney tissues following cisplatin injection, as shown in TEM. Scale bar = 500 nm. E Representative micrographs of CX3CL1 and nephrin staining in kidney tissues. Scale bar = 10 μm. (WT, wild type; KO, knockdown; H&E, hematoxylin and eosin; PAS, periodic acid-Schiff; BUN, blood urea nitrogen; Scr, serum creatinine; WT1, Wilms tumor protein; TEM, transmission electron microscopy; p value was calculated by one-way analysis of variance and Tukey’s test. *p < 0.05, **p < 0.01, and ***p < 0.001 vs. the control group; ^#p < 0.05, ^##p < 0.01, and ^###p < 0.001 vs. the Cis group)