Hellebrigenin, as a selective inhibitor of MAPK signaling pathways (ERK, p38, JNK) and XIAP, effectively suppresses Akt expression and phosphorylation. This compound activates endogenous apoptosis pathways (including mitochondrial membrane potential disruption, Caspase family activation, and PARP cleavage) while modulating apoptosis-related protein expression. Hellebrigenin also induces DNA double-strand breaks to activate the ATM pathway, inhibiting tumor cell proliferation and clonogenesis, primarily applied in research of oral squamous cell carcinoma and liver cancer.

Methods: Oral cancer SCC-1/47 cells and liver cancer HepG2 cells were treated with Hellebrigenin (2-8 nM, 24-72 h), and cell viability was detected by MTT assay. Results: Hellebrigenin inhibited the cell viability of oral cancer SCC-1/47 cells and liver cancer HepG2 cells in a dose- and time-dependent manner. Methods: Oral cancer SCC-1/47 cells were treated with Hellebrigenin (2-8 nM, 24 h), and the expression of related apoptosis proteins was detected by WB. Results: Hellebrigenin induced apoptosis in oral cancer SCC-1/47 cells and activated Caspase-3/8/9 and PARP cleavage, accompanied by upregulation of Bax/Bak and downregulation of Bcl-2/Bcl-xL, Cyclin A2/B1, and CDK4/6. [1]

Methods: Hellebrigenin (6 mg/kg, intraperitoneal injection, three times a week for 4 weeks) was used to treat oral cancer SCC-1 cell xenograft model mice to study its effects on tumor growth and mouse body weight.
Methods: Hellebrigenin significantly inhibited tumor growth in the oral cancer SCC-1 cell xenograft model of mice without affecting mouse body weight. [1]