Phillyrin (Forsythin) is a novel AMPK activator, has anti-obesity effects in nutritive obesity mice, it can prevent lipid accumulation in HepG2 cells by blocking the expression of SREBP-1c and FAS through LKB1/AMPK activation. Phillyrin(Forsythin) may be a new preventive agent of acute lung injury in the clinical setting, it potentially contributes to the suppression of the activation of MAPK and NF-κB pathways, it also has protective effects on H2O2-induced oxidative stress and apoptosis in PC12 cells.

Phillyrin suppressed high glucose-induced lipid accumulation in HepG2 cells. Phillyrin strongly inhibited high glucose-induced fatty acid synthase (FAS) expression by modulating sterol regulatory element-binding protein-1c (SREBP-1c) activation. Moreover, use of the pharmacological AMP-activated protein kinase (AMPK) inhibitor revealed that AMPK is essential for suppressing SREBP-1c expression in Phillyrin-treated cells. Liver kinase B1 (LKB1) phosphorylation is required for the Phillyrin-enhanced activation of AMPK in HepG2 hepatocytes.

Phillyrin has anti-obesity effect in nutritive obesity mice. Phillyrin could lower wet weight of fat (P < 0.01), fat index (P < 0.05 or P < 0.01), the diameter of fat cell and Lee's index (P < 0.05), decrease the jejunum microvillus area, lower the level of serum triglyceride and cholesterol.