Bilberry Anthocyanins (Vaccinium myrtillus L.) Induced Apoptosis of B16-F10 Cells and Diminished the Effect of Dacarbazine

Abstract

Anthocyanins have been reported to have potential as dietary or pharmaceutical supplements in the application of cancer prevention and adjunctive treatment. However, there are few studies on the effect of anthocyanins on melanoma, which have only been performed in cell lines. The objective of this work was to investigate the anticancer effects and mechanisms of bilberry anthocyanin extract (BAE) on melanoma In Vitro and In Vivo. Moreover, a primary study was done to investigate how BAE influenced C57BL/6 mice bearing subcutaneous B16-F10 tumors treated with dacarbazine (DTIC). BAE-induced apoptosis in B16-F10 cells was associated with activation of the mitochondrial pathway induced by increased reactive oxygen species. More, In Vivo anticancer activity studies indicated that BAE attenuated melanoma growth, as identified by hematoxylin-eosin staining, Ki-67, and TUNEL assays. Further western blot results revealed higher phospho-Akt expression with the combination of BAE and DTIC, indicating no suppression of the PI3K/AKT signaling pathway. In summary, this study demonstrated the anti-melanoma activity of BAE and investigated its mechanism. Notably, it should be careful to use products enriching BAE for those melanoma patients treated with DTIC.

Authors Contributions

Yuhua Yue and Shun Feng conceived and designed the experiments; Xuehong Yu and Yuhua Yue performed the experiments; and Xuehong Yu performed the data analyses and interpretation; Haizhu Shi, Kaiyan Xu, and Chungu Zhang contributed to reagents, materials, and analysis tools; Yu Wan, and Xuehong Yu wrote the paper. All authors read and approved the final manuscript. Shun Feng supervised all aspects of the project.

Disclosure Statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

The authors acknowledge the Basic Research programs of Sichuan Province (21YYJC3252); and Central University Basic Research Fund of China (2682020ZT86).