Abstract
ObjectivesWe aimed to investigate the protective effect of Lycium barbarum polysaccharides (LBPs) against oxidative stress–induced apoptosis and senescence in human lens epithelial cells.MethodsTo study apoptosis, SRA01/04 cells, a human lens epithelial cell lines, were exposed to 200 µM hydrogen peroxide (H2O2) for 24 h with or without pretreatment with LBPs. Cell viability was measured using a Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis, intracellular reactive oxygen species (ROS), and the loss of mitochondria membrane potential (Δψm) were detected by flow cytometric analyses. Expression levels of Bcl-2 and Bax proteins were measured by western blot analysis. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were quantized using commercial enzymatic kits according to the manufacturer's instructions. To study senescence, SRA01/04 cells were pre-incubated with LBPs and all cells were then exposed to 100 µM H2O2 for 96 h. Cellular senescence was assessed by morphologic examination and senescence-associated β-galactosidase (SA-β-gal) staining.ResultsLBPs significantly reduced H2O2-induced cell apoptosis, the generation of ROS, the loss of Δψm, and the levels of MDA. LBPs also inhibited H2O2-induced downregulated Bcl-2 and upregulated Bax proteins and increased the levels of SOD and GSH enzyme activity. Moreover, LBPs significantly attenuated H2O2-induced cellular senescence.ConclusionsThese findings suggested that LBPs protect human lens epithelial cells from H2O2-induced apoptosis by modulating the generation of ROS, loss of Δψm, Bcl-2 family, and antioxidant enzyme activity and attenuating cellular senescence.
Highlights
Age-related cataracts, known as senile cataracts, are characterized by the gradual accumulation of cloudy deposits on the ocular lens of the elderly
L. barbarum polysaccharides (LBPs) were demonstrated to protect H2O2-induced breaks in the DNA in mouse testicular [24], liver, and kidney tissue from the oxidative damage caused by streptozotocin-induced diabetic rats [25]; it was not known whether LBPs can protect lens epithelial cells from oxidative stress
SRA01/04 cells were incubated with multiple concentrations of LBPs (0, 50, 100, 200, 400, and 800 mg/L) and showed no significant cytotoxicity; cell cytotoxicity was detected at a concentration of 1600 mg/L LBPs
Summary
Age-related cataracts, known as senile cataracts, are characterized by the gradual accumulation of cloudy deposits on the ocular lens of the elderly. Hydrogen peroxide (H2O2) is the main intracellular ROS in the aqueous humor that can cause protein oxidation and aggregation, lipid peroxidation, and DNA damage, and can decrease antioxidant levels in the lens, eventually accelerating the damage to the lens epithelial cells, resulting in subsequent cataract development [6,7,8]. Based on the antioxidant activity of LBPs, many studies have demonstrated that LBPs have a protective effect against oxidative injury in various cells and tissues. LBPs were demonstrated to protect H2O2-induced breaks in the DNA in mouse testicular [24], liver, and kidney tissue from the oxidative damage caused by streptozotocin-induced diabetic rats [25]; it was not known whether LBPs can protect lens epithelial cells from oxidative stress
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