Honokiol inhibits H2O2-induced apoptosis in human lens epithelial cells via inhibition of the mitogen-activated protein kinase and Akt pathways

Oxidative stress-induced apoptosis in lens epithelial cells plays an important role in cataract formation, and its prevention may be of therapeutic interest. This study was performed to investigate the protective effect and mechanisms of honokiol on H2O2-induced apoptosis in human lens epithelial (HLE) cells. HLE cells (SRA01-04) were pretreated with honokiol at concentrations of 5 μM, 10 μM and 20 μM before 50 μM H2O2 treatment. The results demonstrated that pretreatment of honokiol inhibited the activation of caspase-3 and caspase-9 and downregulated the expression of Bcl-2. Mechanistically, honokiol suppressed H2O2-induced phosphorylation of ERK1/2, p38 mitogen-activated protein kinase (MAPK), JNK and Akt. Honokiol also inhibited H2O2-induced nuclear factor-κB (NF-κB)/p65 phosphorylation and translocation in HLE cells. These results demonstrate that honokiol suppresses H2O2-induced HLE cell apoptosis via interference with the MAPKs, Akt and NF-κB signaling, suggesting that honokiol might have a potential effect against cataract formation.