Li Jun, Wang Peipei, Ying Jia, Chen Zhen, Yu Songping
Department of Ophthalmology, Lishui Hospital affiliated with Zhejiang University, Lishui, PR China.
Cell Physiol Biochem. 2016;39(3):1196-208. doi: 10.1159/000447826. Epub 2016 Sep 5.
Curcumin possesses many pharmacological properties including anti-inflammatory effects. Although prior studies indicate that curcumin has beneficial effects for diabetic retinopathy, the mechanism of action is not known. To address this issue, we investigated the effect of curcumin against diabetes-induced retinal vascular damage and its mechanism of action by using cultured retinal Müller cells stimulated with high glucose.
We studied the effects of curcumin in vivo in the retinas of rats rendered diabetic by streptozotocin and in vitro in Müller cells stimulated with high glucose. We administered curcumin, or KN93, an inhibitor of calcium/calmodulin dependent protein kinase II (CaMKII), or saline vehicle to experimental animals on a daily basis for 12 weeks. Primary cultures of rat Müller cells were incubated with normal glucose or high glucose, with or without curcumin, KN93, or pyrrolidine dithiocarbamate (PDTC), an inhibitor of the transcription protein nuclear factor κB (NF-κB). We examined mRNA and protein levels of vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS) and intercellular adhesion molecule-1 (ICAM-1) by real-time RT-PCR and Western blotting, respectively. Retinal levels of CaMKII and NF-κB were examined by Western blotting. Vascular leakage was evaluated using Evans blue.
Curcumin and KN93 significantly inhibited the activation of CaMKII/NF-κB signaling induced by diabetes or elevated glucose, and subsequently decreased the expression of VEGF, iNOS and ICAM-1. These changes were associated with a decrease of diabetes-induced retinal vascular leakage.
Curcumin protects the diabetic rat retina against early retinal vascular damage, by inhibition of CaMKII activity. Curcumin is currently used to treat a number of clinical conditions, and may prove beneficial for the management of diabetic retinopathy.
姜黄素具有多种药理特性,包括抗炎作用。尽管先前的研究表明姜黄素对糖尿病视网膜病变有益,但其作用机制尚不清楚。为解决这一问题,我们通过使用高糖刺激的培养视网膜穆勒细胞,研究了姜黄素对糖尿病诱导的视网膜血管损伤的影响及其作用机制。
我们研究了姜黄素在链脲佐菌素诱导的糖尿病大鼠视网膜中的体内作用,以及在高糖刺激的穆勒细胞中的体外作用。我们每天给实验动物施用姜黄素、钙/钙调蛋白依赖性蛋白激酶II(CaMKII)抑制剂KN93或生理盐水载体,持续12周。将大鼠穆勒细胞原代培养物与正常葡萄糖或高葡萄糖一起孵育,添加或不添加姜黄素、KN93或转录蛋白核因子κB(NF-κB)抑制剂吡咯烷二硫代氨基甲酸盐(PDTC)。我们分别通过实时逆转录聚合酶链反应(RT-PCR)和蛋白质印迹法检测血管内皮生长因子(VEGF)、诱导型一氧化氮合酶(iNOS)和细胞间粘附分子-1(ICAM-1)的mRNA和蛋白质水平。通过蛋白质印迹法检测视网膜中CaMKII和NF-κB的水平。使用伊文思蓝评估血管渗漏。
姜黄素和KN93显著抑制糖尿病或高糖诱导的CaMKII/NF-κB信号通路的激活,随后降低VEGF、iNOS和ICAM-1的表达。这些变化与糖尿病诱导的视网膜血管渗漏减少有关。
姜黄素通过抑制CaMKII活性,保护糖尿病大鼠视网膜免受早期视网膜血管损伤。姜黄素目前用于治疗多种临床病症,可能对糖尿病视网膜病变的管理有益。