Kommula Sivakesava Rao, Vadakattu Sai Santhosh, Myadara Srinivas, Putcha Uday Kumar, Tamanam Raghava Rao, Palla Suryanarayana
Lipid Chemistry Division, National Institute of Nutrition, Jamai-Osmania, Hyderabad, 500007 India.
Pathology Division, National Institute of Nutrition, Hyderabad, India.
Indian J Clin Biochem. 2020 Oct;35(4):442-450. doi: 10.1007/s12291-019-00842-z. Epub 2019 Jul 9.
Diabetic retinopathy (DR) is one of the major causes of blindness all over the world. According to the previous studies, impaired glucose tolerance (IGT) has been linked to retinal dysfunction/vascular damage. Decreased retinal function is an initial event of early DR. Although the biochemical and molecular events are not fully understood, glial activation, angiogenesis and oxidative stress are some of the pathways associated with early retinal abnormalities. Since IGT is associated with development of retinal dysfunction/vascular damage; as a preventive strategy, we have studied beneficial effect of Cinnamon as a hypoglycaemic agent on long-term IGT induced retinal abnormalities using neonatal streptozotocin (nSTZ) rat model. Control, IGT rats were maintained on AIN-93M diet alone and another set of IGT rats were maintained on AIN-93M diet with 3% Cinnamon for 8 months. At the end of the study, untreated IGT rats developed retinal functional abnormalities as assessed by electroretinogram (ERG) and the retinal structure did not alter as assessed by H&E staining. Further, increase in expressions of GFAP, VEGF and decreased expression of rhodopsin in untreated IGT rat retinas. 4-HNE, a marker of oxidative stress was also elevated in IGT state. Supplementation of Cinnamon to IGT rats had lowered fasting and postprandial glucose levels and also prevented retinal functional abnormalities. Further, Cinnamon protected photoreceptor cell damage, suppressed glial activation, angiogenesis and oxidative stress as there was an improved rhodopsin expression, inhibited elevated expressions of GFAP, VEGF and 4-HNE respectively. In conclusion, Cinnamon attenuated IGT induced retinal abnormalities probably through its hypoglycemic property.
糖尿病视网膜病变（DR）是全球失明的主要原因之一。根据以往的研究，糖耐量受损（IGT）与视网膜功能障碍/血管损伤有关。视网膜功能下降是早期糖尿病视网膜病变的初始事件。尽管生化和分子事件尚未完全明确，但神经胶质细胞激活、血管生成和氧化应激是与早期视网膜异常相关的一些途径。由于IGT与视网膜功能障碍/血管损伤的发生有关；作为一种预防策略，我们使用新生链脲佐菌素（nSTZ）大鼠模型研究了肉桂作为降血糖剂对长期IGT诱导的视网膜异常的有益作用。对照组、IGT大鼠仅维持AIN-93M饮食，另一组IGT大鼠维持AIN-93M饮食并添加3%肉桂，持续8个月。在研究结束时，通过视网膜电图（ERG）评估，未治疗的IGT大鼠出现视网膜功能异常，通过苏木精和伊红（H&E）染色评估，视网膜结构未改变。此外，未治疗的IGT大鼠视网膜中胶质纤维酸性蛋白（GFAP）、血管内皮生长因子（VEGF）表达增加，视紫红质表达降低。氧化应激标志物4-羟基壬烯醛（4-HNE）在IGT状态下也升高。给IGT大鼠补充肉桂可降低空腹和餐后血糖水平，并预防视网膜功能异常。此外，肉桂保护光感受器细胞损伤，抑制神经胶质细胞激活、血管生成和氧化应激，因为视紫红质表达得到改善，分别抑制了GFAP、VEGF和4-HNE的升高表达。总之，肉桂可能通过其降血糖特性减轻IGT诱导的视网膜异常。
