Histidine protects human lens epithelial cells against H2O2-induced oxidative stress injury through the NF-kB pathway

Histidine, an amino acid that is essential to humans, exerts favorable cytoprotective effects against oxidative stress in vivo and in vitro, but the effect of histidine on human lens epithelial cells (HLECs) and its regulatory mechanism have not previously been reported. The oxidative stress induced by H2O2 plays an important role in the pathology of cataract. We know that HLECs are important for maintaining the transparency and integrity of the lens. In the present study, we investigated the possible molecular mechanisms underlying the cytoprotective effects of histidine against H2O2-induced oxidative stress in HLECs. The results showed that histidine reduced H2O2-induced cell apoptosis and reactive oxygen species (ROS) accumulation, protected HLECs from H2O2-induced oxidative damage, increased the expression levels of dismutase (SOD) and glutathione (GSH), and decreased the expression level of malondialdehyde (MDA), and the protective effect of histidine depended on the NF-kB pathway. Together, these data suggest that histidine could be helpful in inhibiting oxidative stress in the lens and thus attenuating cataract formation.