| Aims: Transforming growth factor (TGF)-β1 plays a key role in renal scarring in a wide range of kidney diseases; however, its role in alcoholic nephropathy (AN) has yet to be illustrated. We studied the expression of TGF-β1 and fibronectin in this model, and the effect of fluvastatin on these molecules was also examined.Methods: Male Wister rats randomized into three subgroups and treated daily with saline (VH, 10ml_/kg, gavage twice per day), 400g-L"1 alcohol (AN, 8g ?kg ?d"', gavage twice per day), and alcohol plus fluvastatin (AF, 2mg-kg~1-d~1). Sirius-red staining, immunohistochemistry, electronic microscope were used to examine the expression of TGF-β1 and fibronectin and morphologic changes. Urinary β2-micro-globin and serum cholesterol were also studied with biochemistry and radio-immunology methods.Results: Compared with VH-treated rats, alcohol-treated rats showed mesangial proliferation and matrix deposition, and tubular vacuolation, swelling, obliteration, and tubulointerstitial inflammatory cell infiltration. Sirius red staining displayed a significant increase in collagen in areas of glomeruli, tubulointerstitium, and vessels. Concomitant administration of fluvastatin reversed all of above parameters (P<0.01). Of note, the upregulated expression of TGF-β1 and fibronectin proteins was significantly suppressed by fluvastatin treatment. Serum cholesterol and urinary micro-albumin excretion were increased in the AN group compared with the VH group, but their levels were lowered by fluvastatin, although serum GPT and GOP were unaffected.Conclusions: These findings suggest that the expression of TGF-β1 and fibronectin is upregulated in a rat model of alcoholic nephropathy, and that this is associated with renal scarring. Fluvastatin provides renoprotective effect at least, in part, by downregulating TGF-β1 and fibronectin.
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