title: [Transforming growth factor-β1 induced cellular proliferation and collagen synthesis was mediated by reactive oxygen species in pulmonary fibroblasts].
abstract: OBJECTIVE
  This study will explore whether reactive oxygen species (ROS) is involved in TGF-β1-induced JNK activation, pulmonary fibroblast proliferation and collagen type I and III synthesis.
  
  
  METHODS
  Pulmonary fibroblasts were randomly divided into control (0.4% serum) and TGF-β1 (5 µg/L) groups to detect whether TGF-β1 could induce pulmonary fibroblast proliferation, synthesis of collagen I and III, phosphorylated-JNK (p-JNK) and 8-OHdG (indicator of ROS); while in the part to explore whether NAC (N-acetyl-L-cysteine, antioxidants) has the inhibitory role in TGF-β1-induced pulmonary fibroblast, it did control (0.4% serum), H2O2 (0.1 mmol/L, positive control), H2O2+NAC (10 mmol/L), TGF-β1 (5 µg/L), TGF-β1+NAC groups. Pulmonary fibroblast proliferation, 8-OHdG levels, expressions of JNK and collagen I and III were used by MTT assay, immunofluorescence and western blot respectively.
  
  
  RESULTS
  In the experiments to detect the effect of TGF-β1 on pulmonary fibroblasts, compared with control, TGF-β1 significantly stimulated pulmonary fibroblast proliferation and increased collagen I and III protein, p-JNK and 8-OHdG levels. In the next experiments to explore whether NAC has the inhibitory role in TGF-β1-induced pulmonary fibroblasts, compared with control, pulmonary fibroblast proliferation and the levels of collagen I and II, p-JNK, 8-OHdG were all significantly increased in H2O2 and TGF-β1 groups; while these changes were markedly blocked with the treatment of NAC.
  
  
  CONCLUSIONS
  TGF-β1 induces pulmonary fibroblasts to generate ROS, which contributes to JNK activation and pulmonary fibroblast proliferation as well as collagen synthesis, while ROS inhibition suppresses this effet of TGF-β1 in pulmonary fibroblasts.
authors: Pathology Department, College of Basic Medical Science, Hebei United University, Tanshan 063000, China.
authors: Lishuang
authors: L
authors: Zhao
authors: Pathology Department, College of Basic Medical Science, Hebei United University, Tanshan 063000, China.
authors: Zhongqiu
authors: Z
authors: Wei
authors: Pathology Department, College of Basic Medical Science, Hebei United University, Tanshan 063000, China.
authors: Fang
authors: F
authors: Yang
authors: Pathology Department, College of Basic Medical Science, Hebei United University, Tanshan 063000, China. E-mail: syzxp@sina.com.
authors: Ying
authors: Y
authors: Sun
mesh_terms: D000111:Acetylcysteine; D049109:Cell Proliferation; D003094:Collagen / Q000096:biosynthesis*; D024042:Collagen Type I; D005347:Fibroblasts / Q000166:cytology*; D006861:Hydrogen Peroxide; D008168:Lung / Q000166:cytology*; D020935:MAP Kinase Signaling System; D010766:Phosphorylation; D017382:Reactive Oxygen Species / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism*
chemical_list: D024042:Collagen Type I; D017382:Reactive Oxygen Species; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D003094:Collagen; D006861:Hydrogen Peroxide; D000111:Acetylcysteine