摘要
目的探讨葛根素对实验性高眼压视网膜缺血-再灌注损伤后视神经的保护作用及其机制。方法用眼内灌注法前房灌注林格氏液制成急性高眼压视网膜缺血-再灌注损伤模型。将70只SD大鼠随机分为正常对照组(10只),葛根素治疗组(30只)和模型组(30只)。其中后2组根据再灌注的时间不同分为1d、3d、7d组,每组10只大鼠。治疗组经大鼠腹腔注射葛根素注射液(60mg·kg-1),模型组经大鼠腹腔注射生理盐水(10mL·kg-1)。利用免疫组织化学法检测各组大鼠视网膜内一氧化氮合酶(neural nitrogenoxide synthase,nNOS)的表达,以及硫代巴比妥酸法测量丙二醛(malonaldialdehyde,MDA)含量,黄嘌呤氧化酶法测超氧化物歧化酶(superoxide dismutase,SOD)活性。结果从再灌注1d开始,模型组视网膜内nNOS阳性表达明显增多,MDA水平持续升高,SOD活性持续下降,其差异与正常对照组相比,有统计学意义(P<0.01)。与模型组相比,再灌注各时段葛根素治疗组nNOS阳性神经元明显减少(P<0.01),MDA含量降低(P<0.01),SOD活性升高(P<0.01),其中nNOS阳性神经元与正常对照组相比,无统计学意义(P>0.05)。结论葛根素可通过提高视网膜组织中SOD活性,降低MDA含量,以及增加组织中nNOS表达,对大鼠实验性高眼压视网膜缺血-再灌注损伤有一定的保护作用。
Objective To investigate the protective effect and mechanism of puerarin on optic nervers after experimental retinal ischemia-reperfused injury. Methods Retinal ischemia was induced in SD rats by increasing intraocular pressure through intracameral infusion. Seventy rats were randomly divided into 3 groups： normal control （10 rats）, puerarin treatment（30 rats） and molde group（30 rats）. The latter two groups were subdivided into group 1 day, 3 days and 7 days after reperfusion, respectively, with 10 rats in each group. Puerarin and molde group, respectively. The expression of neural nitrogen oxide synthase （nNOS） was detected by immunohistochemistory. The content of malonaldialdehyde（MDA） and the superoxide dismutase（SOD） activity were measured by spectrophotometer. Results Began from the first day after reperfusion, in saline control group, the histopathological damages of retina were aggravating, the expression of nNOS and the content of MDA were increased, the activity of SOD was decreased persistently, which significantly differed from the normal control group （P 〈0.01）;In contrast to the modle group, the histopathological damages were alleviated, nNOS positive neurons were decreased （P 〈 0.01 ）, decreased MDA content（ P 〈 0.01 ）, and increased SOD activity（P〈 0.01 ）, no statistical significance of nNOS postive neurons was found between the treatment group and normal control group（P 〉 0.05）. Conclusion Puerarin, by increasing SOD activity and the expression of nNOS,decreasing the content of MDA,could protect experimental retinal from ischemia-reperfused injury.
出处
《眼科新进展》
CAS
2006年第12期916-918,共3页
Recent Advances in Ophthalmology
