摘要
目的观察补精益视片对大鼠慢性高眼压(elevated intraocular pressure,EIOP)模型p-Akt表达的干预作用,探讨其作用机理。方法将30只SD大鼠随机分为3组:对照组、模型组、给药组,模型组和给药组采用烙闭上巩膜静脉法建立SD大鼠慢性EIOP模型,给药组每天予1.8 g·kg^(-1)体质量补精益视片混悬液灌胃,对照组、模型组每天予3 mL生理盐水灌胃,连续给药8周,并于8周末处死大鼠,观察各组大鼠眼压、视网膜p-Akt表达的情况。结果模型组、给药组大鼠造模后即刻直至造模后8周与造模前眼压相比均升高,差异均有统计学意义(均为P<0.01);造模后8周眼压与造模后即刻相比,给药组有降低趋势,差异有统计学意义(P<0.01),模型组无降低趋势,差异无统计学意义(P>0.05)。造模后8周视网膜p-Akt表达免疫组织化学分析示:给药组总面积、平均光密度和积分光密度分别为(74 631.81±12 841.30)μm^2,939.26±175.17和37 814.96±5822.71,与模型组的(37 947.26±8050.51)μm^2、481.45±161.02和18 907.64±4367.29相比,差异均有显著统计学意义(均为P<0.01);给药组平均黑度为138.55±8.58,虽高于模型组的136.52±3.81,但差异无统计学意义(P>0.05)。结论补精益视片通过降低眼压、上调视网膜PI3K/Akt信号转导通路中pAkt的表达而保护慢性EIOP模型SD大鼠的视功能。
Objective To observe the effects of bujingyishipian on retinal p-Akt in SD rat model of chronic elevated intraocular pressure(EIOP),and explore the mechanism of it initially.Methods Thirty SD rats were randomly and equally divided into 3 groups:control group,model group and treatment group,10 rats in each group.By unilaterally cauterizing 3 episcleral vessels,the rat model of chronic EIOP was established in model group and treatment group.After given bujingyishipian(1.8 g·kg^(-1),once per day) or normal saline for 8 weeks,the rats were sacrificed.The intraocular pressure(IOP),expression of retinal p-Akt were observed.Results At models building and 8 weeks after-models,IOP was obviously increased by unilaterally cauterizing episcleral vessels(all P〈0.01);IOP was obviously reduced at 8 weeks after-models in treatment group compared models building(P〈0.01),while model group was not statistically significant(P〉0.05).At 8 weeks after-models,the immunohistochemical analysis of retinal p-Akt expression showed that the total area in treatment group was(74 631.81 ± 12 841.30) μm^2,mean optical density was 939.26 ± 175.17,integrated optical density was 37 814.96 ± 5822.71,while the total area in model group was(37 947.26 ± 8050.51) μm^2,mean optical density was 481.45± 161.02,integrated optical density was 18 907.64±4367.29,there were statistical differences between two groups(all P〈0.01).Though mean black degree in treatment group(138.55 ± 8.58)was little higher than model group(136.52±3.81),there was no significant difference in statistics(P〉0.05).Conclusion Bujingyishipian can protect the visual function on the rat model of chronic EIOP by up-regulating the expression of retinal p-Akt and reducing IOP slightly.
出处
《眼科新进展》
CAS
北大核心
2015年第12期1105-1108,共4页
Recent Advances in Ophthalmology
基金
国家自然科学基金资助(编号:81373695/H2713)
成都中医药大学科技发展基金资助(编号:030018024)~~