Zuo Zhong-Fu, Zhang Qiang, Liu Xue-Zheng
Department of Human Anatomy, Liaoning Medical University, Jinzhou 121001, Liaoning Province, China.
Int J Ophthalmol. 2013 Aug 18;6(4):422-4. doi: 10.3980/j.issn.2222-3959.2013.04.02. eCollection 2013.
To explore the effects and potential mechanisms of curcumin on retinal Müller cell in early diabetic rats.
Diabetic rats were induced by a single intraperitoneal injection of streptozotocin (STZ). Male Sprague-Dawley (SD) rats were randomly assigned into 4 groups: control group (naïve SD rats administered with a single intraperitoneal injection of citric buffer), diabetic group (STZ-diabetic rats), dimethyl sulfoxide (DMSO) group (diabetic rats intraperitoneally administered with mixture of DMSO and normal saline, once a day) and curcumin group (diabetic rats intraperitoneally administered with curcumin, 80mg/kg, once a day). Three months after diabetes onset, malondialdehyde (MDA, indication of oxidative stress level) and reduced glutathione (GSH) in retina were detected with kits, glial fibrillary acidic protein (GFAP) in retina was revealed by immunohistochemistry and Western blot, and retinal glutamine synthetase (GS) were observed by Western blot.
Compared with control group, retinal MDA was increased, and GSH was decreased in diabetic and DMSO groups (P<0.05, respectively). While, retinal MDA and GSH in curcumin group showed no difference compared with control group (P>0.05). Furthermore, up-regulation of retinal GFAP and down-regulation of retinal GS were detected in diabetic and DMSO groups, and no alteration could be observed in curcumin group revealed with Western blot. Compared with control group, retinal Müller cells showed significant increase in GFAP immunochemistry staining in diabetic and DMSO groups. Moreover, GFAP-positive staining was decreased in curcumin group compared with diabetic group.
Curcumin inhibits diabetic retinal oxidative stress, protects Müller cell, and prevents the down-regulation of GS in diabetic retina. Therefore, curcumin has a therapeutic potential in the treatment of diabetic retinopathy (DR).
探讨姜黄素对早期糖尿病大鼠视网膜Müller细胞的作用及潜在机制。
通过单次腹腔注射链脲佐菌素（STZ）诱导糖尿病大鼠。将雄性Sprague-Dawley（SD）大鼠随机分为4组：对照组（单纯腹腔注射柠檬酸缓冲液的正常SD大鼠）、糖尿病组（STZ诱导的糖尿病大鼠）、二甲基亚砜（DMSO）组（糖尿病大鼠腹腔注射DMSO与生理盐水的混合物，每日1次）和姜黄素组（糖尿病大鼠腹腔注射姜黄素，80mg/kg，每日1次）。糖尿病发病3个月后，用试剂盒检测视网膜中丙二醛（MDA，氧化应激水平指标）和还原型谷胱甘肽（GSH），免疫组化和蛋白质印迹法检测视网膜中胶质纤维酸性蛋白（GFAP），蛋白质印迹法观察视网膜谷氨酰胺合成酶（GS）。
与对照组相比，糖尿病组和DMSO组视网膜MDA升高，GSH降低（P均<0.05）。而姜黄素组视网膜MDA和GSH与对照组相比无差异（P>0.05）。此外，糖尿病组和DMSO组检测到视网膜GFAP上调和GS下调，蛋白质印迹法显示姜黄素组无变化。与对照组相比，糖尿病组和DMSO组视网膜Müller细胞GFAP免疫化学染色显著增加。此外，姜黄素组GFAP阳性染色较糖尿病组降低。
姜黄素抑制糖尿病视网膜氧化应激，保护Müller细胞，防止糖尿病视网膜中GS下调。因此，姜黄素在糖尿病视网膜病变（DR）治疗中具有治疗潜力。
