Plumbagin ameliorates renal fibrosis by suppressing epithelial-mesenchymal transition.

Renal fibrosis is a common pathological feature of chronic kidney diseases (CKDs), driven by excessive extracellular matrix (ECM) accumulation. Despite its prevalence, therapeutic candidates specifically targeting fibrosis are limited, and the role of renal tubular epithelial cells in fibrosis pathogenesis remains unclear. In this study, we evaluated the anti-fibrotic effects of Plumbagin, a plant-derived natural compound, using a folic acid-induced renal fibrosis model that simulates proximal tubular injury-driven fibrosis. Plumbagin treatment significantly attenuated renal fibrosis in a folic acid-induced model. Furthermore, using the human proximal tubular epithelial cell line HK-2, we assessed EMT, a key fibrosis-promoting biological process, and the expression of fibrosis-related factors. Plumbagin treatment reduced TGF-β-induced EMT and fibrosis-related factor expression in HK-2 cells. In summary, Plumbagin suppresses EMT in renal tubular epithelial cells under fibrotic conditions and alleviates renal fibrosis. These findings highlight the potential of Plumbagin as a therapeutic drug for renal fibrosis and propose a shared therapeutic strategy for CKD patients.