外源性BDNF对急性高眼压后大鼠视网膜ERK1/2磷酸化的影响

为研究脑源性神经生长因子(BDNF)干预对急性高眼压后大鼠视网膜磷酸化的细胞外信号调节激酶(p-ERK1/2)表达变化的影响,本实验将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或溶媒预处理,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-ERK的免疫组织化学染色。结果显示与正常对照相比,单纯高眼压组急性高眼压后p-ERK表达下调(P<0.05),1、3、7d组内核层出现p-ERK阳性细胞;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时p-ERK的表达与正常对照组相似,7d和14d出现了重新分布。此结果提示外源性BDNF可能通过促进急性高眼压后视网膜ERK1/2的活化对受损的视网膜起保护作用。

The expression of P-ERK1/2 receptor in rat retina following acute high intraocular pressure with BDNF pre-treated

To investigate the expression of phospho-extracellular signal-regulated kinase 1/2 (p-ERK1/2) in rat retina following acute high intraocular pressure(HIOP) with brain-derived neurotrophic factor (BDNF) pre-treated. Seventy-two adult rats were randomly divided into acute HIOP group, BDNF pre-treated 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 until b wave of flash electroretinogragh disappeared and such pressure maintained for 60 min. 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-ERK1/2 was used. The results showed that compared to the normal control group, the expression of p-ERK1/2 was decreased significantly(P<0.05)during reperfusion in the acute HIOP group, and we could detect p-ERK1/2 positive cells in the inner nuclear layer of 1, 3 and 7 day groups. The expression of p-ERK1/2 during reperfusion in vehicle control group was similar to those in acute HIOP group. In the BDNF pre-treated HIOP group, the expression of p-ERK1/2 was similar to the normal group at 1, 3 and 7 day following HIOP, but at 7 and 14 day group, there are p-ERK1/2 positive cells appears in the inner nuclear layer. These results indicate that the protective function of exogenous BDNF to injured retina may be involved in promoting the phosphorylation of ERK1/2 the retina.