Oxymatrine ameliorates epithelial mesenchymal transition in IgA nephropathy induced rats.

In this study, we investigated the efficacy of oxymatrine, a phytochemical alkaloid, in reducing inflammation and fibrosis in a rat model of IgA nephropathy (IgAN) through modulation of the TGF-β/SMAD signaling pathway. Thirty Sprague Dawley rats were randomized into control, IgAN, and treatment groups, the latter receiving oxymatrine postinduction of IgAN. Induced by bovine serum albumin, carbon tetrachloride, and lipopolysaccharides, the disease model was validated by immunofluorescence and histopathological analyses, confirming significant renal deposition of IgA and increased fibrosis markers (IL-6, TGF-β, SMAD 3, and α-SMA). Oxymatrine treatment led to a notable decrease in urine protein levels and red blood cells at 10 weeks, suggesting reduced kidney damage. There was no significant impact on the SGOT or SGPT levels, while it reduced the BUN, serum ALB and creatinine levels, indicating minimal hepatotoxicity and renoprotective effects. Histopathology demonstrated preservation of the glomerular diameter in the treatment group. Immunofluorescence and ELISA revealed a reduction in the levels of proinflammatory (IL-6,TNF-α) and profibrotic (TGF-β, SMAD 3, and α-SMA) markers in treated rats, suggesting that oxymatrine has renoprotective effects on the inhibition of pathological EMT processes and fibrosis in IgAN. Our results suggest that oxymatrine is a potential therapeutic agent for IgAN that attenuates disease progression by targeting the TGF-β/SMAD pathways involved in EMT and fibrosis. Further research is warranted to establish long-term efficacy and safety profiles.