PT  - JOURNAL ARTICLE
AU  - YU-SHAN CHEN
AU  - ROU SUN
AU  - WEI-LUNG CHEN
AU  - YU-CHEN YAU
AU  - FEI-TING HSU
AU  - JING-GUNG CHUNG
AU  - CHIA-JUNG TSAI
AU  - CHIA-LING HSIEH
AU  - YING-MING CHIU
AU  - JIANN-HWA CHEN
TI  - The <em>In Vivo</em> Radiosensitizing Effect of Magnolol on Tumor Growth of Hepatocellular Carcinoma
AID  - 10.21873/invivo.11973
DP  - 2020 Jul 01
TA  - In Vivo
PG  - 1789--1796
VI  - 34
IP  - 4
4099  - http://iv.iiarjournals.org/content/34/4/1789.short
4100  - http://iv.iiarjournals.org/content/34/4/1789.full
SO  - In Vivo2020 Jul 01; 34
AB  - 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.