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首页> 外文期刊>Otolaryngology--head and neck surgery: official journal of American Academy of Otolaryngology-Head and Neck Surgery >Sodium nitroprussideitric oxide causes apoptosis in spiral ganglion cells.
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Sodium nitroprussideitric oxide causes apoptosis in spiral ganglion cells.

机译：硝普钠/一氧化氮钠可导致螺旋神经节细胞凋亡。

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OBJECTIVE: In the cochlea, excitatory amino acid receptor overstimulation induces toxicity in spiral ganglion neurons by an unknown mechanism. In the central nervous system, excitatory amino acid-induced toxicity is mediated by nitric oxide, which induces apoptosis in neurons. This study tested the hypothesis that cochlear nitric oxide-mediated toxicity is the result of induction of apoptosis in spiral ganglion neurons. METHODS: The cochleas of 15 gerbils randomly assigned to different groups were perfused for 30 minutes with a test solution of 1 mmol/L sodium nitroprusside, a nitric oxide donor, or a control solution of artificial perilymph. Animals were killed at varying times, including 2, 3, 4, 8, and 18 hours after perfusion. DNA fragmentation or in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling analysis was done on cochleas for detection of apoptosis. RESULTS: Analysis by both techniques demonstrated marked apoptotic cell changes in spiral ganglion neurons of sodium nitroprusside-treated cochleas evident 4 to 8 hours after perfusion, as compared with minimal to no evidence of apoptosis in spiral ganglion neurons of control specimens. CONCLUSIONS: Exposure to high levels of nitric oxide induces apoptosis in spiral ganglion neurons. Because apoptosis is a delayed, potentially reversible cell death pathway, this may present an opportunity for intervention to prevent or attenuate hearing damage induced by excitotoxic stimuli.
机译：目的：在耳蜗中，兴奋性氨基酸受体的过度刺激以未知的机制在螺旋神经节神经元中诱导毒性。在中枢神经系统中，兴奋性氨基酸诱导的毒性由一氧化氮介导，一氧化氮诱导神经元凋亡。这项研究检验了以下假设：耳蜗一氧化氮介导的毒性是螺旋神经节神经元凋亡诱导的结果。方法：随机分入不同组的15只沙鼠的耳蜗用1 mmol / L硝普钠，一氧化氮供体或人工外周淋巴的对照溶液灌注30分钟。在灌注后2、3、4、8和18小时的不同时间处死动物。 DNA片段化或原位末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸-生物素缺口末端标记分析是在耳蜗上进行的，以检测细胞凋亡。结果：两种技术的分析均表明，硝普钠处理的耳蜗的螺旋神经节神经元在灌注后4至8小时明显凋亡，而对照样品的螺旋神经节细胞凋亡极少甚至没有。结论：暴露于高水平的一氧化氮可诱导螺旋神经节神经元凋亡。由于细胞凋亡是一种延迟的，可能是可逆的细胞死亡途径，因此这可能为预防或减轻由兴奋性毒性刺激引起的听力损害提供了干预的机会。

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