Background: Glioma is the most common malignant tumor of the nervous system, which accounts for more than 45% of central nervous system tumors and seriously threatens our health. Because of high mortality rate, limitations, and many complications of traditional treatment methods, new treatment methods are urgently needed. β-Mangostin is a natural compound derived from the fruit of Garcinia mangostana L. and it has anticancer activity in several types of cancer cells. However, the antitumor effect of β-mangostin in glioma has not been clarified. Hence, this study aimed to investigate its therapeutic effects on gliomas.
Materials and Methods: To study the effect of β-mangostin on glioma cells, cell viability assay, reactive oxygen species production, cell cycle, apoptosis, and mitochondrial membrane potential were evaluated in the C6 cell line in vitro. Immunofluorescence and Western blotting were used to analyze protein expression and phosphorylation to study its mechanism of action. A subcutaneous xenograft model was used to investigate the effect of β-mangostin on tumorigenesis in vivo.
Results: We found that β-mangostin can inhibit glioma cell growth and induce oxidative damage in vitro. In addition, it reduces the phosphorylated form levels of PI3K, AKT and mTOR. Furthermore, the phosphorylated form levels of PI3K, AKT and mTOR were increased after the PI3K inhibitor was added. In vivo experiments showed that β-mangostin can inhibit tumor growth as shown by its reduced size and weight.
Conclusion: This study suggests that β-mangostin can inhibit cell proliferation and induce oxidative damage in cells. It is the first study to demonstrate that β-mangostin induces oxidative damage in glioma cells by inhibiting the PI3K/AKT/mTOR signaling pathway.



中文翻译：

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β-Mangostin 对大鼠 C6 胶质瘤细胞的细胞毒和抗增殖作用依赖于通过 PI3K/AKT/mTOR 通路抑制诱导的氧化应激

背景：胶质瘤是最常见的神经系统恶性肿瘤，占中枢神经系统肿瘤的45%以上，严重威胁我们的健康。由于传统治疗方法死亡率高、局限性大、并发症多，迫切需要新的治疗方法。β-Mangostin 是一种源自藤黄果的天然化合物，对多种癌细胞具有抗癌活性。然而，β-山竹素在胶质瘤中的抗肿瘤作用尚未阐明。因此，本研究旨在探讨其对胶质瘤的治疗作用。
材料和方法：为了研究 β-山竹素对胶质瘤细胞的影响，在体外评估了 C6 细胞系中的细胞活力测定、活性氧产生、细胞周期、细胞凋亡和线粒体膜电位。免疫荧光和Western印迹用于分析蛋白质表达和磷酸化以研究其作用机制。使用皮下异种移植模型研究β-山竹素对体内肿瘤发生的影响。
结果：我们发现β-山竹素可以抑制胶质瘤细胞生长并在体外诱导氧化损伤。此外，它还降低了 PI3K、AKT 和 mTOR 的磷酸化形式水平。此外，在添加 PI3K 抑制剂后，PI3K、AKT 和 mTOR 的磷酸化形式水平增加。体内实验表明，β-山竹素可以抑制肿瘤生长，如其减小的尺寸和重量所示。
结论：本研究提示β-山竹素可抑制细胞增殖，诱导细胞氧化损伤。这是第一项证明 β-mangostin 通过抑制 PI3K/AKT/mTOR 信号通路诱导胶质瘤细胞氧化损伤的研究。