急性高眼压兔眼视网膜中过氧亚硝基阴离子的表达及葛根素对其表达的影响

目的探讨过氧亚硝基阴离子在急性高眼压兔眼视网膜中的表达及其损伤机制,并评价葛根素对其表达的影响。方法27只新西兰大白兔,随机分为正常对照组、模型组及治疗组(耳缘静脉注射葛根素),通过前房灌注建立急性高眼压模型,观察视网膜形态学变化,采用原位缺口末端标记法检测高眼压后6、12、247、2 h视网膜中凋亡细胞,应用免疫组织化学方法检测视网膜中过氧亚硝基阴离子的表达。结果模型组6 h时神经纤维层和内丛状层明显水肿,24 h视网膜变薄、神经节细胞变性、核固缩;凋亡细胞于6 h时少量表达,24 h达到高峰,72 h减少;过氧亚硝基阴离子的表达趋势与凋亡细胞一致。治疗组视网膜水肿及神经节细胞变性、核固缩程度较轻;细胞凋亡及硝基酪氨酸的表达趋势同模型组,但表达均明显低于模型组(P<0.05)。结论急性高眼压兔眼视网膜中过氧亚硝基阴离子的表达增多,并参与介导神经节细胞凋亡,葛根素通过其抗氧化作用抑制过氧亚硝基阴离子的表达,在一定程度上保护神经节细胞。

EFFECT OF PUERAIN ON THE EXPRESSION OF PEROXYNITRITE IN RETINA OF RABBITS WITH ACUTE OCULAR HYPERTENSION

Objective To investigate the expression and nerve injury mechanism of peroxynitrite(ONOO-) in retina of rabbits with acute ocular hypertension,and evaluate the effect of puerarin.Methods Twenty-seven New Zealand white rabbits were randomly divided into normal,model and puerarin-treatment groups.The model of acute ocular hypertension was established by perfusing normal saline into anterior chamber.Histopathological change was observed with optical microscope.Apoptosis of retinal cell at 6th,12th,24th and 72th hour after 60 minute ocular hypertension was measured by Tdt-dUTP terminal nick end labeling method.The expression of ONOO-was studied by immunohistochemical method.Results In model group,the edema of nerve fiber layer and inner plexiform layer were severe at 6th hour.Retinal ganglion cells(RGCs) showed vacuolation degeneration and pycnosis at 24th hour.Apoptosis began to appear in a small quantity at 6th hour,reached the peak at 24th hour and began to deline after 24 hours.The trend of changes in ONOO-expression was similar to that of apoptosis.In treatment group,the histopathological injury was lighter than the model group obviously.The trend of expression of ONOO-and apoptosis followed that of the model group,but the expression was less than the above significantly(P<0.05).Conclusion The expression of ONOO-was more in rabbits retina with ocular hypertension and may play a vital role in RGCs apoptosis;purerain has antioxidation effect and may protect RGCs from ocular hypertension injury by inhibiting the effect of ONOO-.