Table 3.

Detailed molecular mechanisms of cepharanthine in cells.

Targets	Detailed Molecular Mechanisms
NF-κB	Inhibits NF-κB activation by blocking the IKK pathway in RAW264.7 cells. Inhibits the phosphorylation of the NF-κB p65 subunit and the degradation of its inhibitor IκBα in lipopolysaccharide-induced mastitis.
Apoptosis	Activates caspase-9, then activates caspase-3/7 and triggers apoptosis. Upregulates the expression of caspase-8/9 and caspase-3/6 in glucocorticoid-resistant Jurkat T cells in vitro.
Cell cycle control	Dose-dependently inhibits the cell cycle progression of Jurkat T cells in the S-phase. Upregulates the expression of cell cycle proteins A2 and B1 but downregulates that of the cell cycle protein D1 in Jurkat T cells. Dose-dependently upregulates p53 and downstream p21.
MAPK	Activates p38, slightly stimulates JNK phosphorylation, and potentially induced apoptosis. Activates oxidative stress and stress-activated kinases JNK1/2, MAPK p38, and ERK and induces chromatin condensation and nuclear fragmentation.
PI3K/Akt/mTOR	Induces apoptosis and autophagy by inhibiting the AKT/mTOR signaling pathway in breast cancer cells. Inhibits the expression of p-PI3K and mTOR on AKT in Jurkat T cells.
P-glycoprotein	Activates the JNK signaling pathway and induces the expression of MDR1 mRNA and P-glycoprotein. Inhibits the efflux function of P-glycoprotein in MOLT-4/DNR cells and downregulates its protein expression.