Graduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan, R.O.C.
Department of Dentistry, Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan, Taiwan, R.O.C.
In Vivo. 2024 Sep-Oct;38(5):2152-2164. doi: 10.21873/invivo.13678.
BACKGROUND/AIM: Oral squamous cell carcinoma (OSCC) presents a significant health challenge, requiring effective treatments. Magnolol, a compound with potential anticancer properties, warrants investigation in OSCC treatment. Here, we aimed to assess the efficacy of magnolol in inhibiting progression of OSCC and to explore the underlying mechanisms of its action.
We evaluated the effect of magnolol on tumor progression using the MOC1-bearing orthotopic model. We examined its impact on pathology and toxicity through hematoxylin and eosin (H&E) staining, immunohistochemistry (IHC), and biochemical analysis. We also investigated the immunoregulatory effects of magnolol in the MOC1-bearing model using flow cytometry.
At high doses, magnolol significantly reduced tumor volume (p<0.0001 for comparisons between treated with magnolol and untreated groups) and weight loss by 70% in vivo. It also induced caspase-dependent apoptosis, evidenced by 2.42-, 2-, and 2.2-fold increases in the expression of caspase-3, -8, and -9, respectively, in mouse tumors treated with high 60 mg/kg of magnolol compared to untreated (p<0.0001 for all comparisons). Magnolol demonstrated no toxicity, maintaining body weight and normal biochemical parameters, including liver and kidney function. Pathological evaluations showed no adverse effects on organs in all treatment groups. Moreover, high doses of magnolol enhanced natural killer cells (by 3%), dendritic cells (20-25%), and cytotoxic T cells (20-40%) while reducing myeloid-derived suppressor cells and regulatory T cells by 1.5 times.
Magnolol demonstrates potential as a therapeutic agent for OSCC, offering antitumor efficacy and immunomodulatory benefits.
背景/目的：口腔鳞状细胞癌（OSCC）是一个重大的健康挑战，需要有效的治疗方法。厚朴酚作为一种具有潜在抗癌特性的化合物，值得在 OSCC 治疗中进行研究。在这里，我们旨在评估厚朴酚抑制 OSCC 进展的疗效，并探讨其作用机制。
我们使用 MOC1 荷瘤原位模型评估厚朴酚对肿瘤进展的影响。我们通过苏木精和伊红（H&E）染色、免疫组织化学（IHC）和生化分析来检查其对病理学和毒性的影响。我们还使用流式细胞术研究了厚朴酚在 MOC1 荷瘤模型中的免疫调节作用。
高剂量的厚朴酚显著降低了肿瘤体积（与未处理组相比，p<0.0001），并使体内 70%的体重减轻。它还诱导了 caspase 依赖性细胞凋亡，在 60mg/kg 高剂量的厚朴酚处理的小鼠肿瘤中，caspase-3、-8 和 -9 的表达分别增加了 2.42、2 和 2.2 倍（所有比较均 p<0.0001）。厚朴酚没有毒性，维持了体重和正常的生化参数，包括肝功能和肾功能。在所有治疗组中，病理评估均未显示对器官有不良影响。此外，高剂量的厚朴酚增强了自然杀伤细胞（增加了 3%）、树突状细胞（20-25%）和细胞毒性 T 细胞（20-40%），同时减少了骨髓来源的抑制细胞和调节性 T 细胞的数量（减少了 1.5 倍）。
厚朴酚具有成为 OSCC 治疗药物的潜力，具有抗肿瘤疗效和免疫调节作用。
