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作 者:蒋丽珠[1] 赵红念[2] 高春燕[3] 李云[2]
机构地区:[1]大理学院临床医学院神经精神病教研室 [2]大理学院附属医院神经内科 [3]大理学院公共卫生学院,大理671000
出 处:《神经解剖学杂志》2009年第6期659-662,共4页Chinese Journal of Neuroanatomy
基 金:国家自然科学基金(30860089)资助项目
摘 要:为了研究脑源性神经营养因子(BDNF)干预对急性高眼压(HIOP)后大鼠视网膜EIK-1磷酸化的影响,本实验将72只成年大鼠随机分为单纯高眼压组、BDNF预处理高眼压组和溶媒预处理高眼压组。BDNF预处理高眼压组和溶媒预处理高眼压组动物左眼于加压前2d分别给予BDNF预处理或溶媒,右眼设为正常对照。各组动物左眼眼压升高至闪光视网膜电图b波消失的临界眼压并维持60min,动物分别存活1、3、7、14d后处死,冰冻切片行p-EIK-1的免疫组织化学染色。结果显示:单纯高眼压组急性高眼压后大鼠视网膜节细胞层p-EIK-1阳性细胞数较正常对照组下调(P<0.05);溶媒预处理高眼压组实验结果与单纯急性高眼压组相似。BDNF预处理高眼压组急性高眼压后1、3、7d组大鼠视网膜节细胞层p-EIK-1阳性细胞数与正常对照组相似,14d组下调(P<0.05)。此结果提示外源性BDNF促进了急性高眼压后视网膜节细胞层EIK-1的活化,节细胞层EIK-1的磷酸化对受损的视网膜有保护作用。To investigate the effect of brain-derived neurotrophic factor(BDNF) pre-treated on the expression of phospho-EIK-1 ( p-EIK-1 ) in rat retina after acute high intraocular pressure( HIOP), seventy-two adult rats were randomly divided into acute HIOP group, BDNF prctreated HIOP group and vehicle pre-treated HIOP group. The left eyes of rats in BDNF pre-treated HIOP group and vehicle pre-treated HIOP group were injected with BDNF or vehicle respectively 2 days before HIOP. The intraocular pressure of all left eyes was increased un- til b wave of flash electroretinogragh (fERG) disappeared and such pressure maintained for 60 minutes. All the right eyes were served as normal control group. The rats were sacrificed after 1,3,7 or 14 days, immunohistochemistry for detecting the expression of p-EIK-1 was used. The results showed that compared to the normal control group, the p-EIK-1 immunopositive cells in ganglion cell layer were de- creased significantly( P 〈 0.05 )during reperfusion in the acute HIOP group. The expression of p-EIK-1 during reperfusion in vehicle con- trol group was similar to those in acute HIOP group. In the BDNF pre-treated HIOP group, the p-EIK-1 immunopositive cells in ganglion cell layer were similar to those of the normal group at 1, 3 and 7 days following HIOP, but at 14 day group p-EIK-1 immunopositive cells in ganglion cell layer were deereased markedly( P 〈0.05 ). These results indicate that the protective function of exogenous BDNF to injured retina may be involved in promoting the phosphorylation of EIK-1 in ganglion eell layer of the retina.
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