一氧化氮和氧自由基诱导视网膜神经节细胞凋亡

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目的 探讨一氧化氮 (NO)和氧自由基 (O- 2 )诱导培养大鼠视网膜神经节细胞 (RGCs)凋亡的作用及 2种作用因素间的关系。方法 体外培养大鼠 RGCs,用细胞形态学变化和 DNA断裂百分率来确定 NO供体 -硝普钠 (SNP)以及 O- 2 产生体系黄嘌呤氧化酶 (XO)和黄嘌呤 (X)所致的RGCs凋亡情况。结果  (1) NO诱导组较对照组的细胞凋亡百分率和 DNA断裂百分率显著增高 ,且与 SNP的浓度相关 ,加入超氧化物歧化酶 (SOD)后可明显抑制 SNP所致的RGCs凋亡 ;(2 ) O- 2 损伤组的结果与 NO损伤组结果相似 ,同时应用 O- 2 和 NO组所致 RGCs的凋亡作用显著高于单独应用 O- 2 组或 NO组。结论  NO和 O- 2 都能诱导培养的RGCs凋亡 ,并且二者之间存在协同作用 Objective To investigate the effects of nitric oxide (NO) and oxygen free radicals (O 2) on the apoptosis of rat retinal ganglion cells (RGCs) and the relationship between the two factors. Methods Rat RGCs were cultured in vitro, and the changes of cell morphology and percentage of DNA cleavage were used to determine the effects of nitric oxide (NO) donor sodium nitroprusside (SNP) and xanthine oxidase (XO) and xanthine RGCs apoptosis. Results (1) The percentage of apoptosis and percentage of DNA cleavage in NO-induced group was significantly higher than that in control group, and was related to the concentration of SNP. Superoxide dismutase (SOD) could significantly inhibit the apoptosis of RGCs induced by SNP. (2) The results of O-2 injury group were similar to those of NO injury group. The apoptosis of RGCs induced by O-2 and NO was significantly higher than that of O-2 or NO alone group. Conclusion Both NO and O-2 can induce the apoptosis of cultured RGCs and there is a synergistic effect between them
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