Mao Jun-Feng, Liu Shuang-Zhen
Department of Ophthalmology, Xiangya Hospital of Central South University, Changsha 410008, Hunan Province, China.
Int J Ophthalmol. 2013;6(1):19-22. doi: 10.3980/j.issn.2222-3959.2013.01.04. Epub 2013 Feb 18.
To investigate the effect of intravitreal injection of DL-alpha-aminoadipic acid (DL-α-AAA) on ocular refractive state and retinal dopamine, transforming growth factor-β2 (TGFβ2), vasoactive intestinal polypeptide (VIP) in guinea pig form-deprived myopia.
Four-week-old pigmented guinea pigs were randomly assigned to 4 groups: normal control, deprivation, deprivation plus DL-α-AAA, deprivation plus saline. Form deprivation was induced with the self-made translucent eye shields, and lasted for 14 days. 8µg DL-α-AAA was injected into the vitreous chamber of deprived eyes. The corneal radius of curvature, refraction and axial length were measured. Retinal dopamine content was evaluated by the high-performance liquid chromatography with electrochemical detection, and TGFβ2 and VIP protein were detected by Western blotting.
Fourteen days of eye occlusion caused the axial length to elongate and become myopic in the form-deprived eyes, with the decrease of retinal dopamine and the increase of TGFβ2 and vasoactive intestinal polypeptide (VIP) protein. Intravitreal injection of DL-α-AAA could inhibit the myopic shift from (-3.65±1.06)D to (-1.48±0.63)D, P<0.01 due to goggles occluding and cause the decrease of retinal TGFβ2 protein in the deprived eyes. However, intravitreal injection of DL-α-AAA had no significant effect on retinal dopamine and VIP protein in deprived eyes. Retinal TGFβ2 protein correlated highly with the ocular refraction (y=-3.34+0.31/x, F=74.75, P<0.001) and axial length (y=8.39-0.02/x, F=48.32, P<0.001) in different treatment groups.
Intravitreal injection of DL-α-AAA is effectively able to suppress the development of form deprivation myopia, which may be associated with retinal TGFβ2 protein in guinea pigs.
研究玻璃体内注射DL-α-氨基己二酸(DL-α-AAA)对豚鼠形觉剥夺性近视的眼屈光状态及视网膜多巴胺、转化生长因子-β2(TGFβ2)、血管活性肠肽(VIP)的影响。
将4周龄有色豚鼠随机分为4组:正常对照组、剥夺组、剥夺加DL-α-AAA组、剥夺加生理盐水组。用自制的半透明眼罩诱导形觉剥夺,持续14天。向剥夺眼玻璃体内注射8μg DL-α-AAA。测量角膜曲率半径、屈光和眼轴长度。采用高效液相色谱电化学检测法评估视网膜多巴胺含量,采用蛋白质免疫印迹法检测TGFβ^2和VIP蛋白。
14天的眼部遮盖导致形觉剥夺眼眼轴伸长并出现近视,视网膜多巴胺减少,TGFβ2和血管活性肠肽(VIP)蛋白增加。玻璃体内注射DL-α-AAA可抑制因眼罩遮盖导致的近视漂移,从(-3.65±1.06)D降至(-1.48±0.63)D,P<0.01,并使剥夺眼视网膜TGFβ2蛋白减少。然而,玻璃体内注射DL-α-AAA对剥夺眼视网膜多巴胺和VIP蛋白无显著影响。不同治疗组中,视网膜TGFβ2蛋白与眼屈光(y=-3.34+0.31/x,F=74.75,P<0.001)和眼轴长度(y=8.39-0.02/x,F=48.32,P<0.001)高度相关。
玻璃体内注射DL-α-AAA能有效抑制形觉剥夺性近视的发展,这可能与豚鼠视网膜TGFβ2蛋白有关。