Effects of S/B Remedy Containing Scutellaria baicalensis and Bupleurum scorzonerifolfium on Hepatic Interleukin-6 Related Signal Transducer and Activator of Transcription 3 Activation in Mice through Cell-Cell Interaction

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  • Lee Chang-Yin
    Institute of Traditional Medicine, School of Medicine, National Yang-Ming University
  • Wang Jir-You
    Institute of Traditional Medicine, School of Medicine, National Yang-Ming University Department of Orthopedic, Taipei Veterans General Hospital
  • Chen Tzu-Chun
    Institute of Traditional Medicine, School of Medicine, National Yang-Ming University
  • Jiang Jeng-Kae
    Division of Colorectal Surgery, Department of Surgery, Taipei Veterans General Hospital
  • Peng Chi-Hao
    Institute of Traditional Medicine, School of Medicine, National Yang-Ming University
  • Kuo Cheng-Deng
    Department of Medical Research and Education, Taipei Veterans General Hospital
  • Chang Wen-Chi
    Laboratory Animal Center, National Yang-Ming University
  • Chiu Jen-Hwey
    Institute of Traditional Medicine, School of Medicine, National Yang-Ming University Division of General Surgery, Department of Surgery, Taipei Veterans General Hospital Department of Surgery, Cheng-Hsiun Hospital
  • Wu Chew-Wun
    Division of General Surgery, Department of Surgery, Taipei Veterans General Hospital

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Signal transducer and activator of transcription 3 (STAT3) plays an important role in regulating interleukin 6 (IL-6) related growth control of the liver. Our previous study demonstrated that a mixture containing Scutellaria baicalensis and Bupleurum scorzonerifolfium (S/B remedy) modulated the growth of hepatocytes during liver regeneration after 2/3 partial hepatectomy. The aim of this study was to investigate whether S/B remedy induced mouse hepatic STAT3 activation directly in hepatocytes or indirectly via non-parenchymal cell–hepatocyte interaction. Direct S/B remedy effects were studied using primarily isolated hepatocytes; while C57BL/6J mice were used to study indirect effects of S/B remedy using gadolinium chloride to deplete Kupffer cells' function. The results showed that S/B remedy and its active constituents did not directly activate growth-related signaling in primarily isolated hepatocytes. However, S/B remedy induced STAT3 and subsequently suppressor of cytokine signaling (SOCS3) activation in mouse liver and increased serum IL-6 level in a dose-dependent manner, which could be partially blocked by pretreatment with gadolinium chloride. Oligonucloetide microarray analysis from S/B remedy-treated peripheral blood leukocytes demonstrated an up-regulation of IL-6 gene expression. We conclude that S/B remedy did not directly induce STAT3 activation in vitro, but induced hepatic IL-6 related STAT3 activation through non-parenchymal cell-hepatocyte interaction in vivo. The results provide important information on the molecular mechanisms of S/B remedy for treatment of human liver diseases.

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