Hellebrigenin

Hellebrigenin is an inhibitor that selectively targets the MAPK signaling pathway (ERK, p38, JNK) and XIAP, and can inhibit Akt expression and phosphorylation. Hellebrigenin can activate endogenous apoptosis pathways (such as mitochondrial membrane potential disruption, Caspase family activation, PARP cleavage), downregulate anti-apoptotic proteins (Bcl-2, Bcl-xL) and upregulate pro-apoptotic proteins (Bax, Bak). Hellebrigenin can also induce DNA double-strand breaks to activate the ATM pathway. Hellebrigenin can inhibit tumor cell proliferation and clone formation, and is mainly used in the study of oral squamous cell carcinoma, liver cancer and other cancers^[1][2]. In Vitro:Cell viability: Hellebrigenin (2-8 nM; 24-72 h) inhibits the cell viability of oral cancer SCC-1/47 cells and liver cancer HepG2 cells in a dose/time dependent manner^[1][2].
Apoptosis: Hellebrigenin (2-8 nM; 24 h) induces oral cancer cells, activated Caspase-3/8/9 and PARP cleavage, accompanied by Bax/Bak upregulation and Bcl-2/Bcl-xL, Cyclin A2/B1, and CDK4/6 downregulation^[1].
Hellebrigenin triggeres a decrease in mitochondrial membrane potential and Caspase cascade reaction in HepG2 cells^[2].
WB verification: Hellebrigenin (8 nM; 24 h) down-regulates the levels of p-ERK/p38/p-JNK and XIAP expression in oral cancer cells, and inhibits Akt phosphorylation in HepG2 cells^[1][2]. In Vivo:Hellebrigenin (6 mg/kg; intraperitoneal injection; 3 times/week; 4 weeks) significantly inhibits tumor growth in the mouse oral cancer SCC-1 cell xenograft model without affecting the mouse body weight^[1].