›› 2008, Vol. 7 ›› Issue (7): 370-374.

• 基础研究 • Previous Articles     Next Articles

Advanced oxidation protein products induce human peritoneal mesothelial cells expressing transforming growth factor-beta 1 via the generation of reactive oxygen species

CHEN Ji-lin, SHI Quan-ming, ZHAO Jiu-yang, ZHANG Yi-ling, ZHANG Li-hua, XU Mao-lan   

  1. 1Department of Nephrology, The Second Affiliated Hospital of Dalian Medcial University, Dalian 116041, 2The School Hospital of Northeast Dianli University, Jilin 132012. Dalian Institute of Chemical Physics,Chinese Academy of Sciences Dalian 116041 China
  • Received:2008-02-26 Revised:1900-01-01 Online:2008-07-12 Published:2008-07-12

Abstract: 【Abstract】 Objective To investigate advanced oxidation protein products (AOPP) on the expression of transforming growth factor-β1 (TGF-β1) in human peritoneal mesothelial cells (HPMCS) in vitro, and the regulatory effect of endogenous reactive oxygen species (ROS) in this process. Method The model of AOPP-human serum albumin (HSA) was prepared in vitro. TGF-β1 in cultured primary HPMCS was measured by ELISA, TGF-β1 mRNA was determined by RT-PCR, and intracellular ROS was assessed by flow cytometry. Result AOPP-HSA induced the secretion and gene expression of TGF-β1 and the increase of intracellular ROS production in cultured HPMCs in a time- and dose-dependent manner (P<0.01). Pretreatment of HPMCs with antioxidant vitamin E and N-acetyl-cyteine inhibited the AOPP-induced ROS production and the secretion and gene expression of TGF-β1 in the cells in a dose-dependent manner (P<0.01). Cells treated with 50μmol/L vitamin E and 10mmol/L N-acetyl-cyteine exhibited the strongest inhibition. Conclusion AOPP induces the expression of TGF-β1 in HPMCs in vitro, which may be mediated, at least partially, by the ROS-dependent cell signaling pathway. Vitamin E and N-acetyl-cyteine significantly inhibit the secretion and gene expression of TGF-β1 via scavenging ROS in HPMCs. The results of this study may provide a therapeutic strategy for the prevention of peritoneal fibrosis.

Key words: Peritoneal mesothelial cells, Transforming growth factor-beta 1, Chronic kidney disease

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