| Background Alcohol abuse can lead to kidney diseases. Transforminggrowth factor-(3 ; (TGF-β )and connective tissue growth factor(CTGF) may play an important role in alcoholic nephropathy, and both are regulated by the renin angiotensin system (RAS). The aim of this study was to investigate the effect of losartan, a angiotensin II type 1 receptor antagonist(AT1RA), on transforming growth factor- 3 and connective tissue growth factor expressions in alcoholic nephropathy in rats.Methods Male adult Wistar rats randomized into three subgroups andtreated daily for 12 weeks as follows: 1) vehicle: rats were treated with normal saline (20ml ·kg ·d ;gavage twicely); 2) alcoholic nephropathy: rats were treated with alcohol (400g 1, Kg ·kg'·d gavage twicely): 3) alcohol+losartan: rats were concomitantly treated with alcohol and losartan (200mg ·L , img ·kg ·d ', gavage). HE staining, Sirius red stai ning, electronic microscope, and immuriohi stochemistry were used to examine histologic changes, collagen fibers deposition, and the expression of TGF-3 1 and CTGF.Results Compared with vehicle treated rats, alcoholic nephropathy ratsshowed tubular vacuolation, granular degeneration, swelling, tubulointerstitial inflammatory cell infiltration, and rarely mesangial proliferation and matrix deposition. Sirius red staining displayed a significant increase in collagen fibers in areas of glomeruli,tubulointerstitium, and vessels. Concomitant administration of losartan reversed all of above parameters (P<0. Ob). Of note, the upregulated expression of TGF- 3 i and CTGF proteins was significantly suppressed by losartan treatment (P<0. 05).Conclusions These findings suggest that alcoholic nephropathy ischaracterized by the tubular granular degeneration, vacuolation, swelling, and tubulointerstitial inflammatory cell infiltration, and this is associated with upregulation of TGF-3: and CTGF. Losartan treatment offers renoprotection by downregulating TGF-P ; and CTGF expressions.
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