Protective effects of active hexose correlated compound in a rat model of liver injury after hepatectomy

Authors

  • Richi Nakatake Department of Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
  • Yoshito Tanaka Department of Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
  • Yosuke Ueyama Department of Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
  • Hirokazu Miki Department of Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
  • Morihiko Ishizaki Department of Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
  • Kosuke Matsui Department of Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
  • Masaki Kaibori Department of Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
  • Tadayoshi Okumura Department of Surgery, Kansai Medical University
  • Mikio Nishizawa Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, Kusatsu, Shiga, Japan
  • Masanori Kon Department of Surgery, Kansai Medical University, Hirakata, Osaka, Japan.

DOI:

https://doi.org/10.31989/ffhd.v6i11.305

Abstract

Background: Recent evidence has indicated that a functional food, active hexose correlated compound (AHCC), has liver-protective effects via suppression of inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF)-α.

Objective: This study aimed to investigate whether AHCC has beneficial effects in a rat model of endotoxin-induced liver injury after partial hepatectomy, in addition to clarifying the mechanisms of action of AHCC.

Methods: Rats were treated with 70% of partial hepatectomy and lipopolysaccharide (PH/LPS) to induce acute liver injury. A normal diet with or without 2% AHCC was administered orally 10 days before 70% hepatectomy. Inflammatory mediators were analyzed.

Results: AHCC improved the survival rate by 70% in PH/LPS rats. AHCC prevented an increase in serum transaminase levels, and histopathological changes and apoptosis in the liver. AHCC reduced iNOS mRNA and protein expression in the liver, resulting in inhibition of nitric oxide production. AHCC also reduced TNF-α, cytokine-induced neutrophil chemoattractant-1, and interleukin-6 mRNA expression, but enhanced expression of interleukin-10. An electrophoretic mobility shift assay with hepatic nuclear extracts demonstrated that AHCC reduced the activation of nuclear factor (NF)-κB induced by PH/LPS treatment.

Conclusion: AHCC inhibits induction of inflammatory mediators, including iNOS and TNF-α, in part through inhibition of NF-κB activation in a rat model of liver injury. Our findings suggest that AHCC prevents postoperative liver failure after liver resection.

Keywords: active hexose correlated compound, inducible nitric oxide synthase, liver injury, nuclear factor-κB, tumor necrosis factor-α

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Published

2016-11-30

Issue

Vol. 6 No. 11 (2016): November 2016

Section

Research Articles

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