Department of Comprehensive Examination for Eye Diseases, Shanxi Eye Hospital, 56 Xinjian Nan Road, Taiyuan 030001, Shanxi, PR China.
Neurosci Lett. 2011 Aug 26;501(2):83-5. doi: 10.1016/j.neulet.2011.06.049. Epub 2011 Jul 3.
Acute stress can provoke apoptosis of the retina cells, and up-regulation of calcitonin gene related peptide (CGRP) in retina. However the role of CGRP in the pathology of the stress induced apoptosis of the retina cells is still elusive. The aim of this study was to investigate the endogenous of CGRP on retinal cell apoptosis induced by the stress of acute myocardial infarction induced by permanent coronary artery occlusion (CAO) in rats. The acute myocardial infarction model was established by ligating the left anterior descending branch of coronary artery in male Sprague-Dawley rats. The rats were randomized into two groups, the CGRP(8-37) group and a control group, pretreated with CGRP(8-37) (10(-7)mol/L, 1 μL/g, intravenously injected), a specific antagonist of CGRP receptor, and 0.9% saline respectively, at 15 min prior to the CAO. The samples of the retina were collected at 3h of CAO for the assays of TUNEL and caspase-3 activity respectively. The total apoptosis ratio of retinal cells in CGRP(8-37) group was significantly higher than that in the control group (P<0.05). The capase-3 activity was significantly greater in the CGRP(8-37) group, compared with the control group (P<0.05) at 3h of CAO. The vacuolar degeneration of retinal ganglion cells was observed in the CAO animals. The results suggest that the endogenous CGRP may play a protective role in the retinal cell apoptosis induced by the stress of acute myocardial infarction.
急性应激可诱发视网膜细胞凋亡，并上调降钙素基因相关肽（CGRP）在视网膜中的表达。然而，CGRP 在应激诱导的视网膜细胞凋亡中的作用仍不清楚。本研究旨在探讨内源性 CGRP 在永久性冠状动脉结扎（CAO）诱导的急性心肌梗死应激诱导的大鼠视网膜细胞凋亡中的作用。通过结扎雄性 Sprague-Dawley 大鼠的左前降支冠状动脉建立急性心肌梗死模型。将大鼠随机分为两组，CGRP（8-37）组和对照组，分别在 CAO 前 15 分钟预先给予 CGRP（8-37）（10（-7）mol/L，1μL/g，静脉注射）和 CGRP 受体的特异性拮抗剂 0.9%生理盐水。在 CAO 后 3 小时采集视网膜样本，分别用于 TUNEL 和 caspase-3 活性检测。CGRP（8-37）组的视网膜细胞总凋亡率明显高于对照组（P<0.05）。与对照组相比，CGRP（8-37）组在 CAO 后 3 小时 caspase-3 活性显著升高（P<0.05）。CAO 动物的视网膜神经节细胞出现空泡变性。结果表明，内源性 CGRP 可能在急性心肌梗死应激诱导的视网膜细胞凋亡中发挥保护作用。
