摘要
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.
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 groups：group1（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（P0.05）,meanwhile,as ischemia prolonged,the expression of Bcl-2 became weaker,and the expression of Bax became stronger gradually（P0.05）.Electrical stimulating cerebellar fastigial nucleus alleviated these changes in treated group（P0.05）.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.
出处
《昆明医学院学报》
2011年第10期41-44,共4页
Journal of Kunming Medical College
关键词
缺血-再灌注
电刺激
小脑顶核
凋亡
TUNEL
Bcl-2
BAX
视网膜
Ischemia-reperfusion injury
Electrical stimulation
Cerebellar fastigial nucleus
Apoptosis
TUNEL
Bcl-2
Bax
Retina
