感觉神经对应激反应诱发的视网膜细胞凋亡的影响

目的 应用实验大鼠模型,观察感觉神经在应激反应诱发视网膜损伤中的作用.方法 采用结扎冠状动脉左前降支的方法制备急性心肌缺血模型;应用辣椒素去乳鼠感觉神经的方法制备去感觉神经大鼠模型.雄性SD大鼠24只(48眼),随机分为两组(每组12只24眼):结扎冠状动脉(CAO)3h和6h组.辣椒素去神经结扎冠状动脉(D-CAO)3h和6h组.采用TUNEL染色技术和caspase-3活性测定观察各组大鼠视网膜细胞凋亡情况.结果 CAO组与D-CAO组比较,TUNEL染色D-CAO各时点组视网膜细胞凋亡水平较CAO相应时点组显著升高(P＜0.001);凋亡主要集中于视网膜神经节细胞层、内核层、外核层及色素上皮层.D-CAO6小时组的总凋亡率明显高于D-CAO3小时组.Caspase-3活性测定D-CAO各时点组较CAO相应时点组活性明显升高(P＜0.01).结论 结扎冠状动脉后,辣椒素去神经大鼠视网膜细胞凋亡水平较未去神经大鼠视网膜细胞凋亡水平明显升高.提示:感觉神经参与了急性心肌缺血伤害性刺激的感受及信息传递和调制,抑制伤害性刺激诱发的神经源性机制的激活及传导过程,感觉神经可能对急性应激反应引发的视网膜组织损伤具有保护作用.

Impact of denervation of capsaicin sensitive sensory afferent nerves on apoptosis of retinal cells

Objective To investigate the impact of acute stress induced by myocardial ischemia on the apoptosis of retina cells in normal rats and the rats with sensory nerve denervated, and to explore the potential protective role of sensory nerve in the pathology. Methods Twenty-four healthy adult male Sprague-Dawley rats (24 eyes), weighing 250-300g, were randomly divided into two groups: coronary artery occlusion (CAO) groups of 3 hour group and 6 hour group. Twelve denervated adult male Spraque-Dawley rats (24 eyes), weighing 250-300g, were randomly divided into denervated coronary artery occlusion (CAO) groups of 3 hour group and 6 hour group. The acute myocardial ischemia model was established by occluding the left anterior descending branch of coronary artery of the rats. The samples were processed for caspase-3 activity detection and TUNEL staining after CAO, as scheduled. Results Retinal edema was seen under the light microscope in CAO group. The apoptotic retinal cells were mainly located in inner nuclear layer, retinal ganglion cell layer, outer nuclear layer, and pigment epithelium. The apoptotic levels of the retinal cells in the animals of D-CAO group were significantly greater, comparing with normal rats in CAO groups (P ＜ 0.01). Conclusions (1) The stress induced by coronary artery occlusion could provoke a significant increase in apoptosis of rat retinal cells, which is mainly located in inner nuclear layer, retinal ganglion cell layer, outer nuclear layer and pigment epithelium. It may indicate that the stress evoked by acute myocardial ischemia, as a nociceptive stimulus,may initiate the pathology of retinal injury. (2) The stress produces a greater apoptosis of rat retinal cells in D-CAO than in CAO animals, which may imply that sensory nerves are involved in the modulation of apoptotic injury of retina.