神经生长因子对青光眼的保护作用与机制探讨

摘要

目的：探讨神经生长因子（ NGF）对青光眼的保护作用及作用机制。方法选取2010年3月至2012年4月广西壮族自治区南溪山医院收治的急性闭角型青光眼术后视神经损伤患者62例，采用随机数字表法分为观察组和对照组，各31例。观察组在术后注射鼠生长因子30μg，每日1次，1个月为1个疗程；对照组静脉滴注长春西汀30 mg，每日1次，2周为1个疗程。治疗后比较两组患者的视力治疗效果、视野恢复效果及血清一氧化氮（NO）和血浆内皮素1（ET－1）水平。结果治疗后，观察组总有效率显著高于对照组（93.6％比61.3％），差异有统计学意义（P＜0.05）；观察组视野恢复总有效率高于对照组（87.1％比61.3％），差异有统计学意义（ P ＜0.05）；观察组治疗后1个月复查血浆ET－1水平低于对照组[（52±13） ng／L比（58±10） ng／L]，血清NO水平高于对照组[（35±10）μmol／L 比（31±8）μmol／L]，差异均有统计学意义（均P＜0.01）。结论 NGF治疗急性闭角型青光眼视神经元损伤的效果优于长春西汀，其视神经保护机制可能与血清 NO 水平下降、血浆ET－1特异性升高有关。%Objective To explore the protective effect and mechanism of nerve growth factor(NGF) to glaucoma.Methods A total of 62 patients with acute angle-closure glaucoma after optic nerve damage admitted to Nanxishan Hospital of Guangxi Zhuang Autonomous Region from Mar .2010 to Apr.2012 were divided into observation group and control group of 31 cases each.The observation group was injected rat growth factor 30 μg,once a day after operation,while the control group received intravenous infusion of vinpo-cetine once a day.After treatment the effects of vision therapy,vision recovery effect and serum NO and plasma endothelin-1(ET-1) levels of the two groups.Results After treatment,the total effective rate of the observation group was significantly higher than the control group(93.6%vs 61.3%),the difference was sta-tistically significant(P <0.05); vision recovery total of the observation group was higher than the control group (87.1% vs 61.3%),the difference was statistically significant (P<0.05);one month after the etre-examination result of plasma ET-1 level of the observation group was lower than the control group[(52 ±13) ng/L vs (58 ±10) ng/L],the serum level of NO was higher than the control group [(35 ±10)μmol/L vs (31 ± 8) μmol/L],the differences were statistically significant (P <0.01).Conclusion The effect of NGF in the treatment of acute angle closure glaucoma optic nerve damage is better than vinpocetine .Its optic nerve protec-tion mechanism may be related to the decreased levels of serum NO and the specific increase of plasma ET-1.