骨肉瘤被认为是原发性恶性骨癌最常见的形式，迫切需要新的治疗选择。 Arnicolide D 是一种从传统中药蜈蚣中提取的倍半萜内酯，对多种癌症具有抗癌功效。然而，其对骨肉瘤的作用尚不清楚。本研究旨在探讨arnicolide D对骨肉瘤细胞MG63和U2OS的抗癌活性及其作用的潜在分子机制。通过MTT法和集落形成实验评估细胞活力和增殖能力不同浓度的arnicolide D处理24 h和48 h。流式细胞术检测arnicolide D处理24 h后细胞周期进展和细胞凋亡。Western blotting测定PI3k、Akt和m-TOR的表达以及我们的研究结果表明，arnicolide D 处理会导致细胞活力显着降低、增殖受到抑制、细胞凋亡诱导以及细胞周期停滞在 G2/M 期。此外，arnicolide D 可以抑制骨肉瘤细胞中 PI3K/Akt/mTOR 通路的激活。根据我们的研究结果，arnicolide D 表现出显着的抗骨肉瘤活性，并有潜力被认为是未来骨肉瘤的治疗候选者。版权©边沁科学出版社；如有任何疑问，请发送电子邮件至 epub@benthamscience.net。

Osteosarcoma is considered as the most prevalent form of primary malignant bone cancer, prompting a pressing need for novel therapeutic options. Arnicolide D, a sesquiterpene lactone derived from the traditional Chinese herbal medicine Centipeda minima (known as E Bu Shi Cao in Chinese), showed anticancer efficacy against several kinds of cancers. However, its effect on osteosarcoma remains unclear.This study aimed to investigate the anticancer activity of arnicolide D and the underlying molecular mechanism of its action in osteosarcoma cells, MG63 and U2OS.Cell viability and proliferation were evaluated through MTT assay and colony formation assay following 24 h and 48 h treatment with different concentrations of arnicolide D. Flow cytometry was employed to examine cell cycle progression and apoptosis after 24 h treatment of arnicolide D. Western blotting was performed to determine the expression of the PI3k, Akt and m-TOR and their phosphorylated forms.Our findings revealed that arnicolide D treatment resulted in a significant reduction in cell viability, the inhibition of proliferation, and the induction of apoptosis and cell cycle arrest in the G2/M phase. Furthermore, arnicolide D could inhibit the activation of PI3K/Akt/mTOR pathway in osteosarcoma cells.Based on our results, arnicolide D demonstrated significant anti-osteosarcoma activity and held the potential to be considered as a therapeutic candidate for osteosarcoma in the future.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.