科研之友
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摘要
TNF-alpha has recently been identified to be a mediator of retinal ganglion cell (RGC) death, while glial cells are relatively protected against this death stimulus. Exposure of RGCs to TNF-alpha is thought to contribute to RGC apoptosis. Apigenin is a flavone with powerful anti-inflammatory properties that exists naturally in various plants and Chinese medicine. In our study, MTT assays showed that apigenin significantly inhibited the decrease of RGC viability induced by TNF-alpha in a dose-dependent manner. Pretreatment with apigenin prevented TNF-alpha-induced apoptosis in a dose-dependent manner as shown by flow cytometry. The production of ATP and the total oxygen uptake were also promoted after apigenin administration. TNF-alpha stimulation led to a significant reduction of bcl-2 and enhancement of bax, which was reversed by apigenin treatment. Apigenin treatment also alleviated the increased caspase-3 activity induced by TNF-alpha. Moreover, luciferase reporter assay indicated that apigenin dose-dependently decreased NF-kappa B activation induced by TNF-alpha, but had no significant effect on activation of AP-1. Collectively, these data demonstrated that apigenin alleviated TNF-alpha-induced apoptosis through inhibition of caspase-dependent apoptotic pathway and activation of nuclear factor-kappaB. Therefore, apigenin may be developed as an anti-apoptotic drug to treat retinopathy.
- 出版日期2014
- 单位上海交通大学
