4.6 Article

Lycium barbarum Polysaccharides Protect Human Lens Epithelial Cells against Oxidative Stress-Induced Apoptosis and Senescence

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PLOS ONE
卷 9, 期 10, 页码 -

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PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0110275

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资金

  1. Guangdong Province Natural Science Fund [S2013010016037]
  2. National Basic Research Program of China (973 program) [2011CB707501]

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Objectives: We aimed to investigate the protective effect of Lycium barbarum polysaccharides (LBPs) against oxidative stress-induced apoptosis and senescence in human lens epithelial cells. Methods: To study apoptosis, SRA01/04 cells, a human lens epithelial cell lines, were exposed to 200 mM 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 (Delta psi m) 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 mM H2O2 for 96 h. Cellular senescence was assessed by morphologic examination and senescence-associated beta-galactosidase (SA-beta-gal) staining. Results: LBPs significantly reduced H2O2-induced cell apoptosis, the generation of ROS, the loss of Dym, 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. Conclusions: These findings suggested that LBPs protect human lens epithelial cells from H2O2-induced apoptosis by modulating the generation of ROS, loss of Delta psi m, Bcl-2 family, and antioxidant enzyme activity and attenuating cellular senescence.

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