〔Abstract〕 Objective To explore effects of serum containing Bailing capsules and reduced glutathione(GSH) on proliferation of rat interstitial fibroblasts NRK-49 F cells and expression level of transforming growth factor-beta1(TGF-β 1) and sma-and mad-related protein(Smad). Methods Rats in unilateral ureteral obstruction group were applied to make drug-containing serum(1.5 g/kg Bailing capsules combined with 300 mg/kg GSH) and drug-free serum. The cells in logarithmic growth phase were divided into normal control group, model group(10 ng/ml TGF-β1), negative control group(10 ng/ml TGF-β1+10% drug-free serum) and drug intervention group(10 ng/ml TGF-β1+10% drug-containing serum). The cell morphology of each group was observed under microscope. The cell proliferation of each group was detected by CCK8. The cell cycle distribution of each group was detected by flow cytometry. The expression of TGF-β1/Smad signaling pathway transcription level of each group was detected by RT-PCR. Western blot was performed to detect expression of TGF-β1/Smad signaling pathway protein level in each group. Results Compared with blank control group, proliferation activity of NRK-49 F cells in model group and negative control group significantly increased(P<0.05), cells in G0/G1 phase significantly decreased(P<0.05) and cells in S phase significantly increased(P<0.05). Expressions of proliferating cell nuclear antigen(PCNA), Cyclin D1,Collagen Ⅰ, α-smooth muscle actin(α-SMA), phosphorylation of Smad2/Smad2(p-Smad2/Smad2) and p-Smad3/Smad3 were significantly up-regulated(P<0.05). Compared with negative control group, proliferation activity of NRK-49 F cells in drug intervention group significantly decreased(P<0.05),cells in G0/G1 phase significantly increased(P<0.05) and cells in S phase significantly decreased(P<0.05). Expressions of PCNA, Cyclin D1, Collagen I, α-SMA, p-Smad2/Smad2 and p-Smad3/Smad3 were significantly down-regulated(P<0.05). Conclusion Serum containing Bailing capsules and reduced glutathione may inhibit renal interstitial fibrosis by inhibiting expression of TGF-β1/Smad.