Metformin Prevents H₂O₂-Induced Senescence in Human Lens Epithelial B3 Cells

Abstract

Background: The primary purpose of this study was to investigate the protective effect of metformin against hydrogen peroxide (H 2 O 2)-induced cellular senescence and to explore the underlying molecular mechanism of lens epithelial cell senescence. Material/Methods: We used H 2 O 2 to establish senescence in human lens epithelial B3 cells. The cells were exposed to H 2 O 2 for different numbers of days to mimic aging. Senescence was assessed by senescence-associated b-galactosidase staining, and the molecular mechanism was assessed by real-time polymerase chain reaction (RT-PCR) and western blot analysis. The cultured cells were exposed to 150 μM H 2 O 2 for 7 days with or without metformin to detect the underlying molecular mechanism of lens epithelial cell senescence. Results: The lens epithelial cells exposed to 150 µM H 2 O 2 for 7 days exhibited senescence. The expression levels of senescence-related markers were increased in H 2 O 2-treated cells. Metformin prevented H 2 O 2-induced cellular senescence in human lens epithelial B3 cells. Conclusions: These findings suggest that senescence marker expression is increased in the cells exposed to H 2 O 2. Metformin protects human lens epithelial B3 cells from H 2 O 2-induced senescence.

Inhibition of Retinal Pigment Epithelial Cell Senescence by Metformin: Implications for the Treatment of Macular Degeneration

“…When ARPE-19 cells were treated with metformin, the increases in both SABG staining and p21 levels were attenuated. The effectiveness of metformin in reducing these two key indicators of cell senescence agrees with previous results showing that metformin inhibits senescence in other types of cells, including senescence produced by reactive oxygen species [23][24][25][26].…”

“…Senescence was induced in the ARPE-19 cells by exposure to the reactive oxygen species, t-BHP. Oxidative stress of cells produced by tBHP, as well as other means, has been shown to induce senescence in a number of types of cells, accompanied by increased SABG staining and elevated p21 levels [6,15,19,26,[33][34][35].…”

“…In addition, it has been shown that metformin does not reduce DNA damage in cells exposed to reactive oxidative species, thus it also may not be preventing telomere loss [36]. Several alternative mechanisms for the antisenescence effects of metformin have been proposed by others, and much additional work will be needed to determine which, or if any, of these are involved [23,24,26,36].…”

“…One of the agents that has been reported to have antisenescence effects is metformin [23][24][25][26][27][28]. Although this drug has been shown to inhibit senescence in a number of types of cells, RPE cells have not yet been examined.…”

Astragalus polysaccharide alleviated hepatocyte senescence via autophagy pathway

“…Apoptosis plays an important role during liver aging and is related to many forms of liver dysfunction and disease 15,16 . The chronic, low‐grade, sterile form of inflammation has been proposed as a mediator of human health span and aging 17 .…”