Apigenin prevents TNF-Î± induced apoptosis of primary rat retinal ganglion cells
Corresponding Author(s) : D-W. Luo
Cellular and Molecular Biology,
Vol. 60 No. 4: Issues 4
TNF-Î± 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-Î± 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-Î± in a dose-dependent manner. Pretreatment with apigenin prevented TNF-Î±-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-Î± 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-Î±. Moreover, luciferase reporter assay indicated that apigenin dose-dependently decreased NF-ÎºB activation induced by TNF-Î±, but had no significant effect on activation of AP-1. Collectively, these data demonstrated that apigenin alleviated TNF-Î±-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.
TNF-Î± apigenin retinal ganglion cells apoptosis NF-ÎºB.