摘要
目的:探讨刺五加对大鼠视网膜急性缺血再灌注损伤的保护作用与机制。方法:Wistar大鼠69只,随机选5只为空白对照组,32只为实验组,32只为对照组。对实验组和对照组分别经前房恒压(100mmHg)灌注生理盐水60min,之后恢复视网膜血流灌注,建立视网膜缺血再灌注损伤的动物模型。造模前6h实验组行刺五加注射液100mg/kgip,并于处理后每日上午给药1次直至处死。对照组以等容量的生理盐水腹腔注射至处死。实验组和对照组每组8只分批于缺血再灌注后6,24,48,72h处死,行视网膜Glu和NO含量测定。结果:缺血再灌注48hGlu和NO含量达到峰值,实验组和对照组与空白对照组相比高(P<0.01);实验组各时点Glu含量低于对照组,其中24,48,72h差异显著(P<0.05)。实验组视网膜NO含量在不同时点与对照组相比明显低(P<0.05)。结论:刺五加注射液可以减少大鼠急性缺血再灌注视网膜Glu产生,对抗谷氨酸产生NO,减轻视网膜缺血再灌注损伤。
AIM： To discuss the neuropertection and mechanism of AS to acute ischemia-reperfusion rats. METHODS： Sixty-nine Wistar rats were divided randomly into three groups： 5 in normal group, 32 in AS group and 32 in ischemia-reperfusion group. Intraocular pressure was raised to 100 mmHg by elevating the normal saline container lasting for 60 minutes. Then, reperfusion of the retinal vascular was undergone. AS with i00 mg/kg was intraperitoneal injected to the rats in AS group six hours before ischemia man- agement and AS rats were given drugs everyday until death. The rats in control group were injected with same volume normal saline. Six, 24, 48, and 72 hours after reperfusion, 8 rats were sacrificed and their eyes were estimated of the level of Glu and NO. RESULTS： By comparing with the normal group, Glu levels were all increased in ischemia-reperfusion group （P〈0.01）. Glu and NO level reached their peak at 48 hours. NO levels of were much higher than that in normal group （P〈0.05）. CONCLUSION： AS can decrease the Glu and antagonize Glu produce NO, decrease the damage of ischemia-reperfusion in retina.
出处
《国际眼科杂志》
CAS
2006年第6期1294-1296,共3页
International Eye Science
关键词
剌五加
谷氨酸
一氧化氮
视网膜保护
acanthopanax senticosus
glutamate
nitric oxide
retina protection
