A study of Leonurine in chemically induced IgA nephropathy on Sprague Dawley rats

IgAN, the most common primary glomerulonephritis, causes nephritic symptoms like blood and protein in urine, elevated creatinine, and chronic kidney inflammation. In this research, we tried to examine the role of phytochemical Leonurine in mitigating fibrosis and inflammation in IgAN rat model through TGF-β/SMAD signalling pathway regulation. Thirty Sprague Dawley rats were randomly assigned to treatment-, control-, and IgAN-induced groups. The treatment-group received Leonurine as a drug post-induction of IgAN. Immunofluorescence and histopathology confirmed the disease model, showing increased fibrosis markers and renal IgA deposits. The model was induced using BSA, CCl4, and LPS. Ten-week leonurine-treatment reduced kidney injury markers, BUN, and serum creatinine in rats without affecting liver enzymes, ameliorating nephritic syndrome without hepatotoxicity. It preserved glomerular diameter and lowered profibrotic and proinflammatory markers. The result indicated that Leonurine ameliorates IgA nephropathy symptoms in rats by reducing inflammation and fibrosis, possibly through TGF-β/SMAD pathways, leading to decreased nephritic symptoms.