Significance statement
Tubulointerstitial fibrosis is an unavoidable consequence of advancing
chronic kidney disease (CKD) and imposes a substantial global health
burden. However, few effective therapeutic agents are available at
present. The present study investigated the ameliorative effects of
icariin on tubulointerstitial fibrosis (TIF) both in vivo andin vitro , and demonstrated that icariin inhibited inflammation
and oxidative stress, at least partially, through improving Nrf2
activity and subsequent mitochondrial function, and eventually mitigated
TIF and preserved renal function, suggesting that icariin could be
developed as a promising therapeutic candidate for the treatment of CKD.