Abstract:Objective To investigate the effect of icariin on renal injury in adriamycin induced nephropathy rats through inflammation fibrosis reaction and its mechanism.Methods Sixty SD rats were randomly divided into model group, prednisone group, ICA group, and combination group, with 12 rats in each group. Prednisone group was given prednisone 6.3 mg/(kg·d), ICA group was given icariin 50 mg/(kg·d), combined group (prednisone + icariin), the blank group, and model group were given 0.9% normal saline 1ml/100g by gavage for 6 weeks. Serum albumin (ALB), urea nitrogen (BUN), and creatinine (Scr) were detected by automatic blood biochemical analyzer, and IL-1 was detected by enzyme-linked immunosorbent assay IL-1β, IL-6, TNF-α, TGF-β, and FN. The expression of SPARC protein was detected by Western blot, and the renal histopathological changes were observed by Masson staining.Results Compared with the blank group, the deposits of glomerular basement membrane in the model group increased gradually, glomerulosclerosis, proliferation of tubulointerstitial fibrous tissue, and extensive interstitial fibrosis were observed; Weight loss, 24 h urine protein increase, ALB, Scr decrease, BUN, IL-1β, IL-6, TNF-α, TGF-β, and FN increased (P < 0.05); SPARC protein expression increased (P < 0.05). Compared with the model group, the above pathological changes in each treatment group were reduced, the body weight increased, the 24-hour urine protein decreased, ALB, Scr increased, BUN, IL-1β, IL-6, TNF-α, TGF-β, FN, and SPARC protein expression decreased (P < 0.05).Conclusion ICA can reduce inflammatory reaction, inhibit fibrosis, and play a protective role on renal injury in rats with adriamycin nephropathy.