Irigenin has been reported to exhibit remarkable anticancer effects against several human cancers. Nonetheless, the anticancer effects of irigenin against the human liver cancer cells are still largely unexplored. Consistently, this study was designed to evaluate the anticancer effects of irigenin against human liver cancer cells and to unveil the underlying molecular mechanisms. The results showed that irigenin significantly (p < 0.05) inhibited the growth of the human HepG2 and SNU-182 liver cancer cells with an IC50 value of 14 µM. Nonetheless, the cytotoxic effects of irigenin against the normal THLE-2 cells were comparatively lower as evident from the IC50 of 120 μM. The AO/EB and DAPI staining showed that irigenin induces apoptosis in the human liver cancer cells. Annexin V/PI staining assay revealed a significant (p < 0.05) increase in the percentage of apoptotic HepG2 and SNU-182 liver cancer cells upon treatment with irigenin. It was found that the number of apoptotic HepG2 and SNU-182 cells enhanced from 2.3 to 41.75% and 1.16 to 51.9% at IC50, respectively. Western blot showed a considerable increase in Bax and decrease in the Bcl-2 expression upon irigenin treatment further confirming the induction of apoptosis. Flow cytometric analysis revealed that irigenin also induces G2/M cell cycle arrest of HepG2 and SNU-182 cells. The percentage of G2/M phase HepG2 and SNU-182 cells increased from 17.92 to 34.35% and 23.97 to 38.23% at IC50, respectively This was also accompanied by decrease in the expression of CDK1 and Cyclin-B in HepG2 and SNU-182 cells. Taken together, the results of the present study suggest that irigenin inhibits the growth of the human liver cancer cells via induction of apoptosis and cell cycle arrest. These results point towards the potential of irigenin as a lead for the development of chemotherapy for liver cancer.

中文翻译：

---

irigenin通过诱导线粒体凋亡和细胞周期阻滞对人肝癌细胞发挥抗癌作用

据报道，鸢尾素对多种人类癌症表现出显着的抗癌作用。尽管如此，irigenin对人肝癌细胞的抗癌作用仍未开发。一致地，本研究旨在评估irigenin对人肝癌细胞的抗癌作用并揭示其潜在的分子机制。结果表明，irigenin显着（p <0.05）抑制人HepG2和SNU-182肝癌细胞的生长，IC50值为14 µM。尽管如此，从120μM的IC50可以看出，irigenin对正常THLE-2细胞的细胞毒性作用相对较低。AO / EB和DAPI染色表明，irigenin诱导人肝癌细胞凋亡。膜联蛋白V / PI染色测定显示显着（p <0。05）用irigenin治疗后，凋亡的HepG2和SNU-182肝癌细胞的百分比增加。发现凋亡的HepG2和SNU-182细胞的数目在IC50下分别从2.3增加到41.75％和从1.16增加到51.9％。Western blot显示，irigenin处理后Bax大量增加，Bcl-2表达减少，进一步证实了细胞凋亡的诱导。流式细胞仪分析表明，irigenin还诱导HepG2和SNU-182细胞的G2 / M细胞周期停滞。在IC50时，G2 / M期HepG2和SNU-182细胞的百分比分别从17.92％增至34.35％和23.97％至38.23％。这还伴随着HepG2和SNU-182细胞中CDK1和Cyclin-B表达的降低。 。在一起 本研究的结果表明，irigenin通过诱导凋亡和细胞周期停滞来抑制人肝癌细胞的生长。这些结果表明，irigenin可能作为开发肝癌化学疗法的先导。