Studies have demonstrated that LBPs have a protective effect against oxidative injury in various cells and tissues. Studies have shown that LBPs significantly alleviate exhaustive exercise-induced oxidative stress in a rat’s skeletal muscle. Another study found that LBPs significantly inhibited oxidative stress and improved arterial compliance in rats. LBPs were also demonstrated to protect H2O2-induced breaks in the DNA in mouse testicular, liver, and kidney tissue from the oxidative damage caused by streptozotocin-induced diabetic rats ; however, it was not known whether LBPs can protect lens epithelial cells from oxidative stress. In the current study, the ability of LBPs to protect against the adverse effects of H2O2 on apoptosis, senescence, cell viability, the generation of ROS, mitochondrial membrane potential, pro-apoptotic proteins, and the level of antioxidant enzymes in human lens epithelial cells was assessed in vitro. Many studies have demonstrated that antioxidants, such as vitamins C and E, and the carotenoid xanthophylls zeaxanthin and lutein might protect against oxidative stress in lens epithelial cells. Here, we systematically investigated the antioxidant activities of LBPs and evaluated their role in H2O2-induced SRA01/04 cell damage. The results showed that treatment with LBPs effectively protected SRA01/04 cells, reduced the generation of ROS and loss of Dym, modulated the expression of Bcl-2 and Bax proteins, and increased antioxidant enzyme activity after H2O2-induced oxidative stress. Oxidative stress–induced apoptosis in lens epithelial cells plays an important role in cataract formation, and its prevention is of therapeutic interest. LBPs, isolated from the aqueous extracts of L. barbarum, have a complicated role in the life and death of cells. Ho et al. investigated whether LBPs could protect neurons against homocysteine excitotoxicity. The results showed that LBPs significantly reduced neuronal cell death and apoptosis induced by Hcy in rat primary culture cortical neurons as Olaparib detected by lactate dehydrogenase assay and caspase-3-like activity assay. In another study the protective effects of LBPs against neuronal cell death were detected in retinal ischemia/reperfusion injuries. Pretreatment with LBPs significantly attenuated neuronal cell apoptosis in the ganglion cell layer and the inner nuclear layer of the I/R retina that was induced by surgical occlusion of the internal carotid artery. Furthermore, LBPs obviously increased the survival rate and promoted the growth of a mixed culture of rat retinal ganglion cells. In the present study, we also demonstrated that LBPs significantly increase the survival of human lens epithelial cells under acute oxidative stress conditions. Under the inverted microscope, SRA01/04 cells exposed to H2O2 exhibited apoptotic-like signs; however, in the presence of LBPs, the proportions of apoptotic cells were significantly decreased. Moreover, flow cytometry analysis showed that LBPs markedly reduced apoptosis in H2O2- treated cells. These indicated that LBPs have a protective effect on cells by inhibiting H2O2-induced cell apoptosis. Apoptosis is a physiological process of cell death that plays a key role in a variety of biologic systems, which has been recognized as providing an important molecular basis for cataracts. The mechanisms for apoptosis involve direct damage to the mitochondria by ROS or indirect mitochondrial depolarization by proapoptotic Bcl-2 family proteins. In this study, H2O2-treated cells showed an increase in intracellular ROS and a loss of Dym and unregulated the expression of Bax and downregulated the expression of Bcl-2; however, the generation of ROS was inhibited by pretreatment with LBPs.