Background and Objective: Renal interstitial fibrosis (RIF) is a prevalent and irreversible process that drives the progression of chronic kidney disease (CKD) to end-stage renal failure and is characterized by significant deposition of fibrotic matrix proteins. The unilateral ureteral obstruction (UUO) model induces rapid tubulointerstitial fibrosis and is widely used to study antifibrotic interventions. Scutellarin, an active flavonoid derived from Erigeron breviscapus, has demonstrated efficacy in alleviating symptoms of various chronic diseases, including stroke, neurodegenerative disorders, and cardiovascular and renal diseases. However, the impact of scutellarin on renal fibrosis in obstructive nephropathy remains unclear. Thus, this study evaluated the effects of scutellarin on fibrosis and renal function in a UUO mouse model. Materials and Methods: Male C57BL/6 mice underwent UUO surgery and received oral scutellarin (21 mg/kg/day) for 3 days before and 5 days after surgery. Renal fibrosis was assessed by immunohistochemistry (IHC; collagen I) and Western blotting (WB; alpha-smooth muscle actin (α-SMA), fibronectin (FN), collagen I). Kidney function was evaluated by urinary protein (BCA assay), serum blood urea nitrogen (BUN), and serum creatinine (Scr). Data were analyzed using GraphPad Prism 8; p < 0.05 was considered statistically significant. Results: UUO induced significant interstitial fibrosis, as evidenced by increased collagen I deposition and elevated protein levels of α-SMA, FN, and collagen I. Scutellarin treatment significantly attenuated these changes, reducing the collagen I IHC-positive area to 0.63-fold and the α-SMA, FN, and collagen I protein levels (WB, normalized to glyceraldehyde-3-phosphate dehydrogenase) to 0.21-, 0.45-, and 0.54-fold of UUO levels, respectively (all p < 0.01). Concurrently, scutellarin significantly lowered proteinuria, BUN, and Scr compared with the UUO group (all p < 0.0001). Conclusion: Scutellarin ameliorated renal fibrosis and dysfunction in the UUO mouse model, associated with downregulation of key fibrosis-related proteins. These findings support further preclinical investigation of scutellarin as a potential antifibrotic agent in kidney disease.
Gong et al. (2026) studied this question.