首页|电刺激大鼠小脑顶核对缺血-再灌注视网膜的保护作用实验研究

电刺激大鼠小脑顶核对缺血-再灌注视网膜的保护作用实验研究

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目的 探讨电刺激大鼠小脑顶核(cerebellar fastigial nucleus,CFN)对视网膜缺血-再灌注损伤的保护作用及其机制.方法 大鼠随机均分为三组,缺血-再灌注损伤组、缺血-再灌注治疗组和假手术组.用TUNEL试剂盒检测视网膜神经节细胞凋亡率;用免疫组织化学染色法检测视网膜细胞Bcl-2蛋白和Bax蛋白的表达.结果 缺血-再灌注损伤可使视网膜神经节细胞发生凋亡(P<0.05),同时视网膜细胞Bcl-2蛋白表达逐渐减弱(P<0.05),Bax蛋白表达逐渐增强(P<0.05);而使用电刺激小脑顶核的治疗组上述改变较轻(P<0.05).结论 电刺激大鼠小脑顶核对视网膜缺血-再灌注损伤具有保护作用,其机制可能通过上调Bcl-2蛋白表达,下调Bax蛋白表达来减少视网膜细胞的凋亡.
Electrical Stimulating Cerebellar Fastigial Nucleus Protects Retina against Ischemia/reperfusion Injury in Rats
Objective To investigate the protective effect and mechanism of electrical stimulating cerebellar fastigial nucleus on retina against ischemia/reperfusion injury in rats. Methods Rats were divided randomly into three groupsrgroupl ( ischemia-reperfusion) , group2 ( electrical-stimulating-treated) , and group3 (sham-operated). Apoptosis of retinal ganglion cells was detected by TUNEL method, and expression of Bcl-2 and Bax were measured by immunohistochemical staining methods. Results Ischemia/reperfusion injury induced the apoptosis of retinal ganglion cells (P<0.05), meanwhile, as ischemia prolonged, the expression of Bcl-2 became weaker, and the expression of Bax became stronger gradually (P<0.05). Electrical stimulating cerebellar fastigial nucleus alleviated these changes in treated group (P <0.05). Conclusions Electrical stimulating cerebellar fastigial nucleus can protect retina against ischemia/reperfusion-injury. The possible mechanism includes upregulating the protein expression of Bcl-2 and downregualting the protein expression of Bax.

Ischemia-reperfusion injuryElectrical stimulationCerebellar fastigial nucleusApoptosisTUNELBcl-2BaxRetina

罗哲文、张虹

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云南省第二人民医院眼科,云南昆明 650021

华中科技大学同济医学院附属同济医院眼科,湖北武汉 430030

缺血-再灌注 电刺激 小脑顶核 凋亡 TUNEL Bcl-2 Bax 视网膜

2011

昆明医科大学学报
昆明医学院

昆明医科大学学报

CSTPCD
影响因子:0.829
ISSN:1003-4706
年,卷(期):2011.32(10)
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