晚期糖基化终产物对C57小鼠耳蜗螺旋神经节细胞凋亡及其受体表达的影响

目的　研究晚期糖基化终产物（advanced glycation end products，AGEs）对体外培养的小鼠耳蜗螺旋神经节细胞（spiral ganglion cells，SGCs）凋亡及晚期糖基化终产物受体（receptor for advanced glycation end products，RAGE）表达的影响，探讨AGEs诱导SGCs凋亡的可能作用途径，分析神经型老年性聋的可能致病机制。方法　运用Tunel法，采用荧光显微镜观察不同浓度、不同时间AGEs对培养的SGCs凋亡的影响，同时用Real time RTPCR方法检测RAGEmRNA表达。结果　AGEs加入细胞培养中，可明显诱导SGCs凋亡，凋亡率与剂量、时间呈正相关。发生凋亡的同时有RAGEmRNA表达增强。结论  AGEs对SGCs有诱导凋亡的作用，该作用可能通过RAGE介导。AGEs促使SGCs凋亡可能是神经型老年性聋的发病机制之一。

Effect of advanced glycation end products on apoptosis of C57 mouse spiral ganglion cells and mRNA expression of advanced glycation end products receptor

OBJECTIVE To analyze the effect of advanced glycation end products(AGEs) on apoptosis of cultured mouse spiral ganglion cells(SGCs) and expression of receptor of AGEs(RAGE). To explore the pathway of AGEs in promoting apoptosis of SGCs. And to explore the possible mechanism of neural presbycusis. METHODS The effect of AGEs on apoptosis of SGCs was studied by Tunel technique and fluorescence microscope. The expression of RAGE mRNA was assayed by Real time RT-PCR. RESULTS AGEs induced apoptosis of cultured SGCs. The effects were dose-dependent and time-dependent. Meanwhile RAGE mRNA expression was enhanced in apoptosis cells. CONCLUSION AGEs induced apoptosis in SGCs,which may be mediated by RAGE. And this may be one of the mechanisms of neural presbycusis.