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 RESEARCH ARTICLE
Year : 2013  |  Volume : 45  |  Issue : 2  |  Page : 174-179

Protection of rhein on IgA nephropathy mediated by inhibition of fibronectin expression in rats


1 Department of Graduate School, Medical College of Nanchang University; Department of Clinical Medicine, Science and Technology School of Jiangxi Traditional Chinese Medicine College, Nanchang, China
2 Department of Histology and Embryology, Medical College of Nanchang University, Nanchang, China
3 Department of Graduate School, Medical College of Nanchang University, Nanchang, China

Correspondence Address:
Zhu Qing-Xian
Department of Histology and Embryology, Medical College of Nanchang University, Nanchang
China
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Source of Support: Jiangxi province science and technology support program, 20111BBG70015-3, Conflict of Interest: None


DOI: 10.4103/0253-7613.108309

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Objective: To investigate the protective effects of rhein on IgA nephropathy (IgAN) in the rat model. Materials and Methods: Twenty-eight female sprague dawley rats were divided randomly into four groups, namely control, IgAN, rhein-prevented and rhein-treated. The pathologic changes on renal tissue were observed by the H and E, staining and the amount of urinary red blood cells and 24-h urinary protein excretion were measured. The glomerular deposition of immune globulin A (IgA) was measured by immunofluorescence staining. Fibronectin (FN) and α-smooth muscle actin (α-SMA) expression on renal tissue were measured via immunohistochemistry. Results: The model of IgAN was established according to Bovine serum albumin-Lipopolysaccharide-Carbon tetrachloride protocol, which was evidenced by histological structural lesions of glomeruli, IgA deposition and urinary measurement. Histological examination of kidney sections from both rhein-prevented group and rhein-treated group showed that glomerular hypertrophy, mesangial expansion, excessive extracellular matrix, and renal capsule dilation were markedly ameliorated compared with IgAN group. Moreover, rhein treatment significantly reduced IgA deposition in glomerulus, the volume of urinary red blood cells and 24-h urinary protein excretion. More importantly, increased FN expression in IgAN was back to normal level in rhein-prevented and rhein-treated group, which was along with the reduction of α-SMA expression in renal tissues. Conclusions: These findings indicate that rhein prevents the development of glomerulosclerosis and halts the progression of IgAN via inhibition of FN and α-SMA expression.






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