The Kampo Medicine Daikenchuto Inhibits Peritoneal Fibrosis in Mice

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  • Kitamura Mineaki
    Second Department of Internal Medicine, Nagasaki University School of Medicine
  • Nishino Tomoya
    Second Department of Internal Medicine, Nagasaki University School of Medicine
  • Obata Yoko
    Second Department of Internal Medicine, Nagasaki University School of Medicine Medical Education Development Center, Nagasaki University Hospital
  • Oka Satoru
    Second Department of Internal Medicine, Nagasaki University School of Medicine
  • Abe Shinichi
    Second Department of Internal Medicine, Nagasaki University School of Medicine
  • Muta Kumiko
    Second Department of Internal Medicine, Nagasaki University School of Medicine
  • Ozono Yoshiyuki
    Department of General medicine, Nagasaki University Graduate School of Biomedical Sciences
  • Koji Takehiko
    Department of Histology and Cell Biology, Unit of Basic Medical Science, Nagasaki University Graduate School of Biomedical Sciences
  • Kohno Shigeru
    Second Department of Internal Medicine, Nagasaki University School of Medicine

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Long-term peritoneal dialysis therapy causes inflammation and histological changes in the peritoneal membrane. Inflammation generally activates fibroblasts and results in fibroblast–myofibroblast differentiation. Heat-shock protein 47 (HSP 47), a collagen-specific molecular chaperone, is localized in myofibroblasts and is involved in the progression of peritoneal fibrosis. Daikenchuto (DKT), a Kampo medicine, is used to prevent postoperative colon adhesion. It inhibits inflammation and HSP 47 expression in the gastrointestinal tract. We examined the effect of DKT on chlorhexidine gluconate (CG)-induced peritoneal fibrosis in mice injected with 0.1% CG dissolved in 15% ethanol. DKT was dissolved in the drinking water. Histological changes were assessed using Masson trichrome staining. Cells expressing α-smooth muscle actin (α-SMA), HSP 47, phospho-Smad 2/3, F4/80, and monocyte chemotactic protein-1 were examined immunohistochemically. Compared with the control group, the peritoneal tissues of the CG group were markedly thickened, and the number of cells expressing α-SMA, HSP 47, phospho-Smad 2/3, F4/80, and monocyte chemotactic protein-1 was significantly increased. However, these changes were inhibited in the DKT-treated group. These results indicate that DKT can prevent peritoneal fibrosis by inhibiting inflammation and HSP 47 expression.

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