Ginsenoside Rh2 is a primary bioactive compound obtained from ginseng that indicated anticancer activities against several malignant tumors. However, previous studies have reported little about the inhibitory effect of Rh2 on osteosarcoma (OS). This study aims to explore whether Rh2 could exert anticancer effects in OS cells and further investigate the proliferation, migration, and apoptosis mechanisms induced by Rh2 in human OS U20S cell line. The viability of U20S cells was obtained by the 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2‐H‐tetrazolium bromide assay. Cell migration property was analyzed by wound‐healing assay. Apoptosis was visualized using terminal deoxynucleotidyl transferase dUTP nick‐end labeling (TUNEL), 4′,6‐diamidino‐2‐phenylindole (DAPI), and annexin V/propidium iodide (PI) staining. Relative protein expressed was confirmed through Western blot analysis. Mitochondrial membrane potential was evaluated by JC‐1 staining. In this study, we used broad‐spectrum anticancer drug cisplatin (CP) as a positive control. The results indicated that Rh2 remarkably inhibited cell viability of U20S cells in a dose‐ and time‐dependent manner, and suppressed migration. TUNEL, DAPI, annexin V/PI, and JC‐1 assay suggested that Rh2 could induce cellular apoptosis. Rh2 could reduce the levels of Bcl‐2, caspase 3, and caspase 9, and promote the expression level of Bax in U20S cells. Moreover, Rh2 could induce apoptosis by promoting mitogen‐activated protein kinase (MAPK) signaling pathway and inhibit PI3K/Akt/mTOR and nuclear factor‐κB (NF‐κB) signaling pathway in U20S cells. These findings indicated that Rh2 has an anticancer effect on U20S cells by regulating MAPK, PI3K/Akt/mTOR, and NF‐κB signaling pathway.

中文翻译：

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人参皂苷Rh2通过调节骨肉瘤细胞中的NF-κB，MAPK和PI3K / Akt / mTOR信号传导通路来阻止增殖和迁移并诱导凋亡。

人参皂苷Rh2是从人参中获得的主要生物活性化合物，对多种恶性肿瘤具有抗癌活性。但是，以前的研究报道很少有Rh2对骨肉瘤（OS）的抑制作用。这项研究旨在探讨Rh2是否可以在OS细胞中发挥抗癌作用，并进一步研究Rh2诱导的人OS U20S细胞系的增殖，迁移和凋亡机制。通过3-（4,5-二甲基-2-噻唑基）-2,5-二苯基-2-H-溴化四氮唑测定获得U20S细胞的活力。通过伤口愈合分析法分析细胞迁移特性。使用末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL），4'，6-二mid基-2-苯基吲哚（DAPI）和Annexin V /碘化丙啶（PI）染色观察细胞凋亡。通过蛋白质印迹分析确认了表达的相对蛋白。通过JC-1染色评估了线粒体膜电位。在这项研究中，我们使用了广谱抗癌药顺铂（CP）作为阳性对照。结果表明，Rh2以剂量和时间依赖性方式显着抑制U20S细胞的细胞活力，并抑制迁移。TUNEL，DAPI，膜联蛋白V / PI和JC-1分析表明Rh2可以诱导细胞凋亡。Rh2可以降低Bcl-2，caspase 3和caspase 9的水平，并促进Bax在U20S细胞中的表达水平。此外，Rh2可以通过促进有丝分裂原激活的蛋白激酶（MAPK）信号通路来诱导细胞凋亡，并抑制U20S细胞中的PI3K / Akt / mTOR和核因子κB（NF-κB）信号通路。