Zhang Z, Liu Y Y, Liu Y, Li Q, Liang T T, Hong F, Feng L, Sun Y
Department of Pathology, School of Basic Medical Science, North China University of Science and Technology, Tangshan 063210, China; Department of Respiratory Medicine, Tangshan Works Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, China.
Department of Respiratory Medicine, Tangshan Works Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2020 Jan 20;38(1):7-12. doi: 10.3760/cma.j.issn.1001-9391.2020.01.002.
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.
探讨过氧化物还原酶2（Prx2）过表达对转化生长因子-β1（TGF-β1）诱导的成纤维细胞增殖及胶原合成的影响。将成纤维细胞随机分为对照组（DMEM培养基）、TGF-β1组（5μg/L TGF-β1）、阴性对照组（用5μg/L TGF-β1处理并转染空慢病毒载体）和Prx2组（用5μg/L TGF-β1处理并转染Prx2过表达慢病毒载体）。采用MTT法检测细胞增殖，免疫荧光法检测8-羟基脱氧鸟苷（8-OHdG）表达，蛋白质印迹法检测磷酸化c-Jun氨基末端激酶（p-JNK）、磷酸化p38丝裂原活化蛋白激酶（p-P38）、Ⅰ型胶原、Ⅲ型胶原及Prx2的表达。采用SPSS 18.0软件进行统计学分析。计量资料以均数±标准差表示，多组间比较采用方差分析，两组间进一步比较采用最小显著差法检验。慢病毒转染成功，Prx2组Prx2蛋白表达显著升高（<0.05）。与对照组比较，TGF-β1组增殖能力显著增强（<0.05）；与TGF-β1组比较，Prx2组增殖能力显著降低（<0.05）。与对照组比较，TGF-β1组8-OHdG、p-JNK、p-P38、Ⅰ型胶原及Ⅲ型胶原表达显著升高（<0.05）；与TGF-β1组比较，阴性对照组8-OHdG、p-JNK、p-P38、Ⅰ型胶原及Ⅲ型胶原表达差异无统计学意义（>0.05），而Prx2组上述指标显著降低（<0.05）。Prx2过表达通过抑制活性氧并激活JNK和P38通路，抑制TGF-β1诱导的成纤维细胞增殖及胶原合成。
