Department of Radiation Oncology, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.
Department of Medical Imaging, Taipei Medical University Hospital, Taipei, Taiwan, R.O.C.
In Vivo. 2020 Jul-Aug;34(4):1789-1796. doi: 10.21873/invivo.11973.
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.
We established a Hep3B bearing mouse to evaluate the efficacy of the combination treatment of magnolol and RT.
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.
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.
背景/目的:我们之前的研究报道了放射性治疗(RT)诱导肝癌(HCC)中的 ERK/NF-κB,这会削弱 RT 的毒性或引发放射抵抗效应。因此,将 RT 与合适的 NF-κB 抑制剂联合使用可能会使 HCC 对 RT 敏感。厚朴酚是一种具有抗炎和抗肿瘤功能的生物活性化合物。在此,我们旨在研究厚朴酚是否可以增强 HCC 体内 RT 的抗肿瘤疗效。
我们建立了一个 Hep3B 荷瘤小鼠模型,以评估厚朴酚与 RT 联合治疗的疗效。
最显著的是,联合组的肿瘤体积和重量抑制效果最为明显。肿瘤免疫组织化学染色也表明,厚朴酚抑制了 RT 诱导的 ERK/NF-κB 相关蛋白的表达。此外,内在凋亡相关蛋白,如 caspase-3 和 -9,在联合组中明显增加。
厚朴酚可能通过下调 ERK/NF-κB 相关蛋白的表达和增加凋亡相关蛋白的表达,有效增强 RT 对 HCC 的抗肿瘤能力。