Abstract
Objective Oxidants play an important role in many diseases, including hearing loss. We hypothesized that (−)-epigallocatechin-3-gallate (EGCG) would protect spiral ganglion cells (SGCs) from H2O2-induced oxidizing damage.
Material and Methods SGCs of postnatal day 1–3 mice were cultured in vitro. H2O2 and EGCG were used at various concentrations. The apoptotic rate of SGCs was evaluated using Hoechst 33 258 staining, and cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide method. Semi-quantitative reverse transcriptase polymerase chain reaction was used to observe manganese superoxide dismutase (MnSOD) gene expression of SGCs treated with H2O2 and EGCG.
Results The viability of cultured SGCs was significantly decreased, and the apoptotic rate of SGCs significantly increased, at H2O2 concentrations ≥50 μM compared with the control (p<0.05). MnSOD gene expression was upregulated with increasing H2O2 concentration in cultured SGCs, while this upregulation was suppressed by EGCG.
Conclusion It is suggested that EGCG, as an antioxidant, significantly protects auditory neurons against H2O2-induced oxidative damage.
Xie DH, Liu GH, Zhu GH, Wu WT, Ge SL. (−)-Epigallocatechin-3-gallate protects cultured spiral ganglion cells from H2O2-induced oxidizing damage. Acta Otolaryngol 2004; 124: 464–470.
Xie DH, Liu GH, Zhu GH, Wu WT, Ge SL. (−)-Epigallocatechin-3-gallate protects cultured spiral ganglion cells from H2O2-induced oxidizing damage. Acta Otolaryngol 2004; 124: 464–470.