[The effect of peroxiredoxin 2 on transforming growth factor-β1-induced fibroblast proliferation and collagen synthesis].

To investigate the effect of peroxiredoxin 2 (Prx2) overexpression on fibroblast proliferation and collagen synthesis induced by transforming growth factor-β1 (TGF-β1) . Fibroblasts were randomly divided into control group (DMEM medium) , TGF-β1 group (5 μg/L TGF-β1) , negative control group (treated with 5 μg/L TGF-β1 and transfected with empty lentiviral vector) , and Prx2 group (treated with 5 μg/L TGF-β1 and transfected with Prx2 overexpression lentiviral vector) . MTT assay was used to measure cell proliferation, immunofluorescence assay was used to measure the expression of 8-OHdG, and Western blot was used to measure the expression of p-JNK, p-P38, collagen type I, collagen type III, and Prx2. SPSS 18.0 was used for statistical analysis. The continuous data were expressed as mean±standard deviation; an analysis of variance was used for comparison between groups, and the least significant difference -test was used for further comparison between two groups. Lentiviral transfection was performed successfully, and the Prx2 group had a significant increase in the protein expression of Prx2 (<0.05) . Compared with the control group, the TGF-β1 group had a significant increase in the proliferation ability (<0.05) , and compared with the TGF-β1 group, the Prx2 group had a significant reduction in the proliferation ability (<0.05) . Compared with the control group, the TGF-β1 group had significant increases in the expression of 8-OHdG, p-JNK, p-P38, collagen type I, and collagen type III (<0.05) ; compared with the TGF-β1 group, the negative control group had no significant changes in the expression of 8-OHdG, p-JNK, p-P38, collagen type I, and collagen type III (>0.05) , while the Prx2 group had significant reductions in the above parameters (<0.05) . Prx2 overexpression inhibits fibroblast proliferation and collagen synthesis induced by TGF-β1 through inhibiting reactive oxygen species and activating the JNK and P38 pathways.