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作 者:张俊琦[1] 邢达勇[2] 刘志英[2] 刘太平[3] 王林洪[2]
机构地区:[1]开滦总医院范各庄医院眼科,河北省唐山市063000 [2]河北联合大学附属医院眼科 [3]中国人民解放军第255医院眼科中心
出 处:《河北医药》2013年第23期3531-3532,共2页Hebei Medical Journal
摘 要:目的观察氨基胍(aminoguaniding,AG)在兔视神经损伤后对视网膜超氧化物歧化酶(SOD)、丙二醛(MDA)含量的影响,研究对视网膜神经节细胞(retinal ganglion cell,RGC)的保护性作用机制。方法健康成年大耳白兔66只,随机分为正常对照组、损伤对照组和损伤治疗组,损伤组按损伤后1 d、3 d、7 d、14 d、21 d分5组,每组6只。损伤组采用同一反向动脉夹夹闭视神经法制作动物模型。伤后2 min耳缘静脉注射2%AG溶液(损伤治疗组)及等量0.9%氯化钠溶液(损伤对照组),测定视网膜组织中SOD、MDA的含量。结果正常视网膜组织中含有一定量的MDA、SOD,视神经损伤后MDA含量逐渐升高,而SOD活力逐渐下降,至伤后14 d时达到高峰,同一时间点损伤对照组和损伤治疗组比较差异有统计学意义(P<0.05)。结论兔视神经损伤后,AG通过对抗自由基的途径减少视神经损伤诱导的RGC凋亡。Objective To observe the effect of aminoguanidine (AG) on the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in retina after optic nerve injury, and to investigate the mechanism of protective effect of AG on retinal ganglion cell (RGC) in rabbits. Methods Sixty-six healthy adult rabbits were randomly divided into three groups:normal control group, injury control group and treatment group. The 30 rabbits in injury group were divided into five groups according to the survival time after injury,which were 1 d,3d ,7d, 14d and 21d groups, with 6 rabbits in each group. The animal models with optic nerve injury were established by clipping optic nerve with artery clamp forceps. Then the rabbits in injury treatment group were injected 2% AG through ear-border vein 2min after injury, however, the rabbits in injury control group were injected equivalence 0.9% sodium chloride solution. The concentrations of SOD and MDA in retina were detected. Results There existed some MDA and SOD in normal retina tissue. The MDA content was gradually increased after optic nerve injury, however,the activity of SOD was gradually decreased, which reached peak at 14d after injury, moreover, there were significant differences at the same time points between injury control group and treatment group ( P 〈 0.05 ). Conclusion After optic nerve injury in rabbits, AG can decrease RGC apoptosis due to optic nerve injury through the way of resisting free radical.
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