Bushen recipe and its disassembled prescriptions inhibit inflammation of liver injury associated with Concanavalin A through Toll‑like receptor 3/9 signaling pathway

Mol Med Rep. 2018 Aug;18(2):1682-1691. doi: 10.3892/mmr.2018.9082. Epub 2018 May 29.

Abstract

The aim of the present study was to explore the effect of Bushen recipe and its disassembled prescriptions on liver injury and chronic hepatitis B. Liver injury was induced in normal and hepatitis B virus (HBV)‑transgenic mice through injection of Concanavalin A, followed by treatment with Bushen recipe and its disassembled prescriptions including the Bushen‑yang, the Bushen‑yin and the QingHua groups as well as the GanYanLing group (positive control). Subsequently, their liver function indexes were investigated by a microplate method and liver sections were blindly evaluated using an optical microscope by a pathologist. Subsequently, the activation state of Toll‑like receptor (TLR)3/9 signaling pathway in liver tissues was analyzed by western blotting. Additionally, the inflammatory factors produced following liver injury in peripheral blood were detected via ELISA. Following intervention with the Bushen recipe and its disassembled prescriptions, the liver function indexe alanine aminotransferase had declined, whereas cholinesterase increased. The pathological alterations of liver tissue in HBV transgenic mice were reversed by Bushen recipe and its disassembled prescriptions. In addition, the TLR3/9 signaling pathway in liver tissues of HBV transgenic mice was inhibited and inflammatory factors such as interleukin (IL)‑6, IL‑1, tumor necrosis factor‑α and interferon‑γ were reduced significantly. In conclusion, the present study demonstrated that Bushen recipe and its disassembled prescriptions repaired liver injury induced by Concanavalin A through inhibition of TLR3/9 signaling pathway.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Chemical and Drug Induced Liver Injury / drug therapy*
  • Chemical and Drug Induced Liver Injury / genetics
  • Chemical and Drug Induced Liver Injury / immunology
  • Chemical and Drug Induced Liver Injury / pathology
  • Concanavalin A
  • Drugs, Chinese Herbal / pharmacology*
  • Gene Expression Regulation
  • Genome*
  • Hepatitis B virus / genetics
  • Interferon-gamma / antagonists & inhibitors
  • Interferon-gamma / genetics
  • Interferon-gamma / immunology
  • Interleukin-1 / antagonists & inhibitors
  • Interleukin-1 / genetics
  • Interleukin-1 / immunology
  • Interleukin-6 / antagonists & inhibitors
  • Interleukin-6 / genetics
  • Interleukin-6 / immunology
  • Male
  • Mice
  • Mice, Transgenic
  • Signal Transduction
  • Toll-Like Receptor 3 / antagonists & inhibitors
  • Toll-Like Receptor 3 / genetics*
  • Toll-Like Receptor 3 / immunology
  • Toll-Like Receptor 9 / antagonists & inhibitors
  • Toll-Like Receptor 9 / genetics*
  • Toll-Like Receptor 9 / immunology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology
  • Virus Integration

Substances

  • Anti-Inflammatory Agents
  • Bushen formula
  • Drugs, Chinese Herbal
  • Interleukin-1
  • Interleukin-6
  • TLR3 protein, mouse
  • Tlr9 protein, mouse
  • Toll-Like Receptor 3
  • Toll-Like Receptor 9
  • Tumor Necrosis Factor-alpha
  • interleukin-6, mouse
  • Concanavalin A
  • Interferon-gamma