Podocin Antibody - #DF8593

Fig3f

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.

Fig. 3 Melittin alleviates podocyte damage and autophagy inhibition in 5/6 Nx rats. A 5/6 Nx of renal failure was established on rats. The rats were then administered low (25 μg/kg body weight), intermediate (50 μg/kg body weight), or high (100 μg/kg body weight) doses of melittin via intraperitoneal injection. Four weeks after the administration, kidney tissues were collected from the rats for assessment. (A) Podocin and (B) nephrin expression levels in the kidney tissues were assessed by qRT-PCR. Expression levels of (C, D) podocin, (C, E) nephrin, (C, F) Beclin 1, (C, G) LC3II/LC3I, and (C, H) p-mTOR/mTOR in the kidney tissues assessed by Western blot.

Figure 2. Effect of YB on HG-induced expression of nephrin, podocin and CD2AP in podocytes. A-C. Podocytes were treated with HG and YB for 24 hours and then mRNA levels of nephrin, podocin and CD2AP were determined by qRT-PCR. (*P