The overactivation of NF-κB caused by the blockage of SIRT1 promotes the generation of ROS, forming an oxidative stress-inflammation positive feedback loop, exacerbating renal damage, testicular spermatogenesis disorders, and sperm DNA damage (Suleiman et al., 2020; Yuan et al., 2022).Previous research has shown that treatment with the SIRT1 agonist BF175 in CKD mice significantly attenuates NF-κB activation and the expression of senescence and inflammatory markers, thereby reducing albuminuria and the progression of CKD (Feng et al., 2021). This evidence concerns the gene NFKB1 and chronic kidney disease.