AIM: To investigate the relative mechanisms of signal transduction of isopsoralen(ISR)and ecdysterone(ECR)on phosphorylated extracellular signal-regulated kinase(p-ERK)expression in human lens epithelial cells(HLEC), which will provide a view in better understanding the mechanisms of aged cataract, and provide the experiment bases for the prophylaxis and treatment of aged cataract.

METHODS:Human lens epithelial cells(HLECs)were cultured and sub-cultured in vitro. The cultured HLECs were exposed to H₂O₂ at 300μmol/L over a time course of several hours, with and without pretreatment with β-Estradiol(E₂), ECR, ISR. The HLECs were used for following experiments. The changes of the expression levels of ERK phosphorylation in HLECs which exposed to H₂O₂, with pretreatment with certain concentration of ECR and ISR, were analyzed by flow cytometer(FCM), the signal transduction mechanism of ECR and ISR on antioxidative damage was studied.

RESULTS: The expression levels of ERK phospho- rylation were examined in normal HLECs by FCM,and peaked at 6 hour. The p-ERK levels of H₂O₂ group gradually decreased with a prolongation of treatment time. There were significant differences as compared with control group respectively(P<0.01). The p-ERK levels of E₂ group gradually increased with a prolongation of treatment time, showed significant increase from 6 hour when compared with H₂O₂ group respectively(P<0.01), and peaked at 6 hour. The p-ERK levels of ECR group showed significant increase from 3 hour when compared with H₂O₂ group respectively(P<0.01), and peaked at 12 hour. The p-ERK levels of ISR group showed significant increase from 1 hour when compared with H₂O₂ group respectively(P<0.01), and peaked at 1 hour.

CONCLUSION:The resistance against oxidant-induced injury by E₂, ECR and ISR in HLECs might relate to ERK/MAPK signaling pathway.