Li Xiaoyan, Zhang Maonian, Zhou Huanfen
Department of Ophthalmology, The First Affiliated Hospital of Chinese PLA General Hospital, 51 Fucheng Road, Haidian District, Beijing 100048, China.
Department of Ophthalmology, PLA General Hospital, 28 Fuxing Road, Haidian District, Beijing 100853, China.
J Diabetes Res. 2014;2014:678123. doi: 10.1155/2014/678123. Epub 2014 Jan 2.
This paper aims to explore the relationship of retinal neuron apoptosis and manganese superoxidase dismutase (MnSOD) at early phase of diabetic retinopathy. Sprague-Dawley rats were grouped into normal controls and diabetics. Data were collected after 4, 8, and 12 weeks (n = 12). The pathological changes and ultrastructure of the retina, the apoptosis rate of retinal neurons by TdT-mediated dUTP nick end label (TUNEL), mRNA expressions of MnSOD and copper-zinc superoxide dismutase (Cu-Zn SOD), and the activities of total SOD (T-SOD) and subtypes of SOD were tested. For the controls, there was no abnormal structure or apoptosis of retinal neurons at any time. There was no change of structure for rats with diabetes at 4 or 8 weeks, but there was a decrease of retinal ganglion cells (RGCs) number and thinner inner nuclear layer (INL) at 12 weeks. The apoptosis ratio of RGCs was higher than that of the controls at 8 and 12 weeks (P < 0.001). The activity and mRNA levels of MnSOD were lower in diabetics at 4, 8, and 12 weeks (P < 0.05). In summary, the apoptosis of the retinal neurons occurred at 8 weeks after the onset of diabetes. Retinal neuron apoptosis in early diabetic rats may be associated with the decreased activity and mRNA of MnSOD.
本文旨在探讨糖尿病视网膜病变早期视网膜神经元凋亡与锰超氧化物歧化酶（MnSOD）之间的关系。将Sprague-Dawley大鼠分为正常对照组和糖尿病组。在4周、8周和12周后收集数据（n = 12）。检测视网膜的病理变化和超微结构、通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法（TUNEL）检测视网膜神经元的凋亡率、MnSOD和铜锌超氧化物歧化酶（Cu-Zn SOD）的mRNA表达以及总超氧化物歧化酶（T-SOD）和超氧化物歧化酶亚型的活性。对于对照组，在任何时候视网膜神经元均无异常结构或凋亡。糖尿病大鼠在4周或8周时结构无变化，但在12周时视网膜神经节细胞（RGCs）数量减少且内核层（INL）变薄。在8周和12周时，RGCs的凋亡率高于对照组（P < 0.001）。在4周、8周和12周时，糖尿病大鼠的MnSOD活性和mRNA水平均较低（P < 0.05）。综上所述，糖尿病发病8周后视网膜神经元发生凋亡。早期糖尿病大鼠视网膜神经元凋亡可能与MnSOD活性和mRNA降低有关。
