Vol.45, No.4, 2021, pp.943-951, doi:10.32604/biocell.2021.015836
OPEN ACCESS
ARTICLE
Hellebrigenin induces apoptosis in colorectal cancer Cells through induction of excessive reactive oxygen species
  • CHUNJIAO LIU1,2, QINHONG KONG1,2, FENG PAN1,2, SHAN JIANG1,2, LINGJIE MENG1,2, GAI HUANG1,2, LIDAN LU1,2, SANHUA LI1,2,*, YUN LIU1,2,3,*
1 Guizhou Provincial College-based Key Laboratory for Tumor Prevention and Treatment with Distinctive Medicines, Zunyi Medical University, Zunyi, 563000, China
2 Life Sciences Institute, Zunyi Medical University, Zunyi, 563000, China
3 Department of Biochemistry and Molecular Biology, Zunyi Medical University, Zunyi, 563000, China
* Address correspondence to: Sanhua Li, ; Yun Liu,
Received 18 January 2021; Accepted 20 February 2021; Issue published 22 April 2021
Abstract
Traditional Chinese medicine (TCM) has been increasingly applied in both preventing and treating a variety of cancers in the last decades, attributing to its fewer side effects as compared with chemotherapy drugs. Hellebrigenin, a component of Chanpi from the skin of Bufo bufogargarizans Cantor or Duttaphrynus melanostictus has been reported to have an obvious anti-cancer activity on various cancers. However, the effect and mechanism of hellebrigenin on colorectal cancers were still unknown. Herein, the present study demonstrated hellebrigenin significantly reduced viability and triggered apoptosis via the intrinsic pathway in colorectal cancer cell lines HCT116 and HT29 in vitro and in vivo. Moreover, hellebrigenin led to a reduction of mitochondrial membrane potential. In addition, treatment with hellebrigenin could result in the induction of excessive reactive oxygen species, which led to cell apoptosis. These results indicated that hellebrigenin had anti-cancer potential in the treatment of colorectal cancers.
Keywords
Hellebrigenin, Colorectal cancer, Reactive oxygen species, Apoptosis
Cite This Article
LIU, C., KONG, Q., PAN, F., JIANG, S., MENG, L. et al. (2021). Hellebrigenin induces apoptosis in colorectal cancer Cells through induction of excessive reactive oxygen species. BIOCELL, 45(4), 943–951.
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