Abstract:【Abstract】 Objective To investigate the effect of sulforaphane on mesangial cell proliferation in nephrotic syndrome rats through transforming growth factor (TG-β)/Smad3 signaling pathway and its mechanism. Methods The proliferation of rat glomerular mesangial cells (HBZY-1) was induced by 2 μ m TGF-β. The cells were divided into control group, TGF-β stimulation group, TGF-β combined with 20 μ m sulforaphane group and TGF-β combined with 40 μ m sulforaphane group. The rat model of nephrotic syndrome was induced by 5 mg/kg adriamycin. Different doses of sulforaphane were used to treat HBZY-1 cells and nephrotic syndrome rats. The rats were divided into blank control group, adriamycin 〖JP〗stimulation group, adriamycin combined with 30 mg/kg sulforaphane group and adriamycin combined with 60 mg / kg sulforaphane group, 8 rats in each group. The proliferation of HBZY-1 cells was detected by CCK8 method, mesangial matrix deposition was analyzed by HE staining, and the expression of FN, col4, TGF-β and P Smad3 were detected by Western blotting. Results TGF-β stimulation group can induce the proliferation of HBZY 1 cells and the expression of FN and col4 protein in HBZY-1 cells, which is statistically significant compared with the blank control group (P<0.05). Compared with TGF-β stimulated group, TGF-β combined with 20 and 40 μ m sulforaphane group could significantly inhibit the proliferation of HBZY1 cells and the expression of FN and col4 protein induced by TGF-β (P<0.05). Adriamycin induced mesangial matrix deposition in rats with nephrotic syndrome increased (P<0.05), while different doses of sulforaphane could significantly reduce mesangial matrix deposition (P<0.05). Adriamycin stimulation group could significantly induce the increase of creatinine, urea nitrogen and 24hour proteinuria, and the expression of FN, col4, TGF-β, p-Smad3 protein in kidney tissue of rats, which was statistically significant compared with the blank control group (P<0.05). Compared with the adriamycin group, different doses of sulforaphane could significantly reduce the levels of creatinine, urea nitrogen, 24hour proteinuria, FN, col4, TGF-β, pSmad3 protein expression in renal tissue (P<0.05). Conclusion Sulforaphane could inhibit the expression of matrix synthesis related proteins by down regulating TGF-β/Smad3 signal transduction, and then reduce the proliferation of mesangial cells in nephrotic syndrome rats.