Effect Of Advanced Glycosylation End Products(AGEs) On Apoptosis Of C57Mouse Spiral Ganglion Cells (SGCs) And MRNA Expression Of AGEs Receptor

Objective：To explore the pathway of advanced glycation end products(AGEs) in promotingapoptosis of cultured mouse spiral ganglion cells（SGCs），effects impacting on theexpression of receptor of AGEs(RAGE) and mechanismofneural presbycusis.Methods：C57BL/6J newborn mice,3~5days after birthwereenrolled,SGCs of themicewere culturedby cutting separation-enzyme digestion method. The SGCs wereidentifiedbyimmunofluorescence with the NF-H as the firstantibody.And RAGE ofSGCswereidentifiedbyimmunofluorescenceand immunohistochemistrywith theanti-RAGE.After4-day-cultured cells were treatedwith different concentrations andtime of AGEs, apoptosis rateswere observedby TUNEL, mRNA expressionof RAGEwas detectedby Real time RT-PCR.Results:The cytoplasm and the nucleus of SGCs produced a green fluorescent byimmunofluorescence with the NF-H as the firstantibody.The cytoplasm and thenucleus of SGCs had a positive reaction by immunofluorescence andimmunohistochemistry with the anti-RAGE, producing a green fluorescent and browncolor respectively. AGEs promoteSGCs apoptosisapparently. The effects weredose-dependent and time-dependent. Meanwhile RAGE mRNA expression wasenhanced in apoptosis cells.Conclusions：RAGE express in the SGCs of newbornmice. AGEs promoteSGCs apoptosis,which may be mediated by RAGE. And this may be one of the mechanisms of the neuralpresbycusis.