Liu Lihua, Zuo Zhongfu, Lu Sijing, Liu Aihua, Liu Xuezheng
Department of Anatomy, Histology and Embryology, Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning 110847 People's Republic of China.
Department of Anatomy, Jinzhou Medical University, Jinzhou, Liaoning 121001, People's Republic of China.
Iran J Basic Med Sci. 2017 Jul;20(7):813-821. doi: 10.22038/IJBMS.2017.9017.
Naringin, an essential flavonoid, inhibits inflammatory response and oxidative stress in diabetes. However, whether naringin has beneficial effects on diabetic retinopathy (DR) remains unknown.
Streptozotocin (STZ, 65 mg/kg) was intraperitoneally injected into male rats (8 weeks old weighting 200-250 g) to establish diabetic model, then naringin (20, 40 or 80 mg/kg/day) was intraperitoneally injected into the diabetic rats for twelve weeks. Glial fibrillary acidic protein (GFAP) level, thickness of ganglion cell layer (GCL) and ganglion cell counts were assessed in diabetic retina . Naringin (50 μM) that significantly inhibited high glucose (HG, 25 mM)-induced cell proliferation was used to treat rat Muller cell line (rMC1) . Inflammatory response, oxidative stress and activation of nuclear factor kappa B (NF-κB) p65 were evaluated in retina and in rMC1 cells .
Naringin alleviated DR symptoms as evidenced by the increased retinal ganglion cells and decreased GFAP level in rat retina. Naringin exhibited anti-inflammatory and antioxidative effects as confirmed by the down-regulated pro-inflammatory cytokines, tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), and the up-regulated antioxidants, glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) in DR rats. Moreover, we found that naringin inhibited HG-induced proliferation, abnormal inflammatory response and oxidative stress in rMC1 cells. In addition, the enhanced nuclear translocation of NF-κB p65 in diabetic rat retina and HG-induced rMC1 cells was suppressed by naringin.
Naringin attenuates inflammatory response, oxidative stress and NF-κB activation in experimental models of DR.
柚皮苷是一种重要的类黄酮，可抑制糖尿病中的炎症反应和氧化应激。然而，柚皮苷对糖尿病视网膜病变（DR）是否具有有益作用仍不清楚。
将链脲佐菌素（STZ，65mg/kg）腹腔注射到雄性大鼠（8周龄，体重200 - 250g）中以建立糖尿病模型，然后将柚皮苷（20、40或80mg/kg/天）腹腔注射到糖尿病大鼠中，持续12周。评估糖尿病视网膜中的胶质纤维酸性蛋白（GFAP）水平、神经节细胞层（GCL）厚度和神经节细胞计数。使用显著抑制高糖（HG，25mM）诱导的细胞增殖的柚皮苷（50μM）处理大鼠穆勒细胞系（rMC1）。评估视网膜和rMC1细胞中的炎症反应、氧化应激以及核因子κB（NF-κB）p65的激活情况。
柚皮苷减轻了DR症状，表现为大鼠视网膜中神经节细胞增加和GFAP水平降低。柚皮苷表现出抗炎和抗氧化作用，这在DR大鼠中促炎细胞因子肿瘤坏死因子α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）下调以及抗氧化剂谷胱甘肽（GSH）、超氧化物歧化酶（SOD）和过氧化氢酶（CAT）上调中得到证实。此外，我们发现柚皮苷抑制rMC1细胞中HG诱导的增殖、异常炎症反应和氧化应激。另外，柚皮苷抑制了糖尿病大鼠视网膜和HG诱导的rMC1细胞中NF-κB p65增强的核转位。
柚皮苷可减轻DR实验模型中的炎症反应、氧化应激和NF-κB激活。
