Mao Junfeng, Liu Shuangzhen, Fu Chunyan
Department of Ophthalmology, Xiangya Hospital, Changsha, Hunan 410008, China
Department of Ophthalmology, Xiangya Hospital, Changsha, Hunan 410008, China.
Exp Biol Med (Maywood). 2016 Jun;241(11):1258-63. doi: 10.1177/1535370216638773. Epub 2016 Mar 14.
The retinal dopaminergic system is involved in the myopic shift following form deprivation. Citicoline has been demonstrated to stimulate the dopaminergic system in the brain and retina. Furthermore, citicoline has been used in many neurogenic diseases, such as senile cognitive impairment, stroke and Parkinson's disease as well as in amblyopia and glaucoma. Our aim was to investigate the effect of citicoline on the refractive state and retinal dopamine level in form deprivation myopia of guinea pigs. Guinea pigs, at an age of four weeks, were randomly divided into normal control, deprivation, deprived + citicoline and deprived + vehicle groups. Form deprivation myopia was induced by a translucent eye shield covering the right eye. Citicoline was injected intraperitoneally twice a day (500 mg/kg, 9 am and 9 pm) for 10 days. In vitro, retinal explants were cultured with citicoline for 24 h, with a final citicoline concentration of 100 µmol/L. The ocular refractive parameters and retinal dopamine content were measured. After occlusion for 10 days, the form-deprived eyes became myopic with an increase in axial length and a decrease in retinal dopamine content. The intraperitoneal injection of citicoline reduced the myopic degree (from -3.25 ± 0.77D to -0.62 ± 0.47D, P < 0.001) and partially raised retinal dopamine levels (from 0.55 ± 0.21 ng to 0.81 ± 0.24 ng, P < 0.01) in the form-deprived eyes. After 24 h of culturing retinal explants with citicoline, retinal dopamine content increased significantly (from 0.42 ± 0.14 ng to 0.62 ± 0.21 ng, P < 0.05). These results demonstrated that an intraperitoneal injection of citicoline could retard the myopic shift induced by form deprivation in guinea pigs, which was mediated by an increase in the retinal dopamine levels.
视网膜多巴胺能系统参与了形觉剥夺后的近视性移位。已证实胞磷胆碱可刺激大脑和视网膜中的多巴胺能系统。此外，胞磷胆碱已被用于多种神经源性疾病，如老年认知障碍、中风和帕金森病，以及弱视和青光眼。我们的目的是研究胞磷胆碱对豚鼠形觉剥夺性近视的屈光状态和视网膜多巴胺水平的影响。4周龄的豚鼠被随机分为正常对照组、剥夺组、剥夺 + 胞磷胆碱组和剥夺 + 赋形剂组。通过用半透明眼罩覆盖右眼诱导形觉剥夺性近视。胞磷胆碱每天腹腔注射两次（500 mg/kg，上午9点和晚上9点），共10天。在体外，将视网膜外植体与胞磷胆碱培养24小时，最终胞磷胆碱浓度为100 μmol/L。测量眼屈光参数和视网膜多巴胺含量。遮盖10天后，形觉剥夺眼出现近视，眼轴长度增加，视网膜多巴胺含量降低。腹腔注射胞磷胆碱可降低形觉剥夺眼的近视度数（从 -3.25 ± 0.77D降至 -0.62 ± 0.47D，P < 0.001），并部分提高视网膜多巴胺水平（从0.55 ± 0.21 ng升至0.81 ± 0.24 ng，P < 0.01）。用胞磷胆碱培养视网膜外植体24小时后，视网膜多巴胺含量显著增加（从0.42 ± 0.14 ng升至0.62 ± 0.21 ng，P < 0.05）。这些结果表明，腹腔注射胞磷胆碱可延缓豚鼠形觉剥夺诱导的近视性移位，这是由视网膜多巴胺水平的增加介导的。
