The In Vivo Radiosensitizing Effect of Magnolol on Tumor Growth of Hepatocellular Carcinoma

In Vivo. 2020 Jul-Aug;34(4):1789-1796. doi: 10.21873/invivo.11973.

Abstract

Background/aim: Radiation (RT) induced ERK/NF-κB in hepatocellular carcinoma (HCC) has been reported in our previous works; it weakens the toxicity of RT or triggers a radioresistance effect. Thus, combining RT with a suitable NF-κB inhibitor may sensitize HCC to RT. Magnolol, a bioactive compound, was known to have anti-inflammatory and anti-tumor functions. Here, we aimed to investigate whether magnolol may enhance anti-HCC efficacy of RT in vivo.

Materials and methods: We established a Hep3B bearing mouse to evaluate the efficacy of the combination treatment of magnolol and RT.

Results: Most significantly, tumor volume and tumor weight inhibition was found in the combination group. Tumor immunohistochemistry staining also illustrated the suppression of RT-induced ERK/NF-κB-related proteins expression by magnolol. In addition, intrinsic apoptosis-related proteins, such as caspase-3 and -9, were markedly increased in the combination group.

Conclusion: Magnolol may effectively enhance anti-HCC ability of RT by downregulating the expression of ERK/NF-κB-related proteins and increasing the expression of apoptosis-related proteins.

Keywords: Magnolol; apoptosis; hepatocellular carcinoma; radiation.

MeSH terms

  • Animals
  • Apoptosis
  • Biphenyl Compounds / pharmacology
  • Carcinoma, Hepatocellular* / drug therapy
  • Cell Line, Tumor
  • Lignans* / pharmacology
  • Liver Neoplasms* / drug therapy
  • Mice
  • NF-kappa B / genetics
  • Radiation-Sensitizing Agents* / pharmacology

Substances

  • Biphenyl Compounds
  • Lignans
  • NF-kappa B
  • Radiation-Sensitizing Agents
  • magnolol