苏林达克
衰老
氧化应激
细胞
黄斑变性
化学
药理学
脂褐素
氧化磷酸化
细胞生物学
生物
生物化学
医学
眼科
非甾体
作者
Samuel P. Manoharan,Herbert P. Weissbach,Shailaja Allani
标识
DOI:10.1096/fasebj.2022.36.s1.r4248
摘要
Age-related macular degeneration (AMD) is the leading cause of blindness in industrialized countries. One of the potential contributors to AMD pathology is retinal pigment epithelial (RPE) cell senescence. Through experimental trial, it is shown that sulindac, an FDA approved non-steroidal anti-inflammatory drug, protects normal cells such as retinal, cardiac, and neuronal cells against oxidative damage through a preconditioning mechanism. The hypothesis is that sulindac can mitigate RPE cell senescence because of its cellular protective properties. To test this, in vitro, an RPE senescence model was established using tert-butyl hydrogen peroxide (TBHP) as an oxidizing agent. The cells were treated with TBHP for 12 hours followed by further incubation for four days. Senescence cells were identified using a Beta-galactosidase assay. The effect of sulindac on senescence was determined by pre-treating cells with varying concentrations of sulindac for 24 h prior to TBHP treatment. Treatment with TBHP induces senescence in the RPE cells under the conditions used. The Preliminary data shows that there was a reduced number of senescent cells in the samples treated with sulindac compared to the control groups. These findings indicate that oxidative damage induces cell senescence, and sulindac can lower the amount of senescence by protecting the RPE cells from oxidative damage. To summarize, the results suggest that sulindac can be used as a therapeutic agent targeting senescence induced by oxidative damage.
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