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叶黄素对链脲佐菌素诱导的糖尿病大鼠白内障的影响。

Effect of luteoin in delaying cataract in STZ-induced diabetic rats.

机构信息

Department of Ophthalmology, The People's Hospital of Binzhou City, Binzhou, 256610, Shandong Province, China.

出版信息

Arch Pharm Res. 2017 Jan;40(1):88-95. doi: 10.1007/s12272-015-0669-5. Epub 2015 Oct 13.

DOI:10.1007/s12272-015-0669-5
PMID:26459282
Abstract

Luteolin, a flavonoid rich in many plants, has shown various pharmacological effects including anti-inflammation, anti-oxidant, anti-tumor, cardioprotective and neuroprotective properties. At present, inflammation and oxidative stress have been recognized to be two important contributing factors to the development of diabetic cataract. The aim of this study is to investigate the effects of luteolin on diabetes-induced oxidative stress and inflammation in the lens of rats. A diabetic rat model was induced by intraperitoneally giving streptozotocin at a dosage of 60 mg/kg, and then the rats were treated by orally administration of luteolin 25, 50 and 100 mg/kg for 12 weeks. The results showed that luteolin administration could increase the antioxidant capacity such as glutathione (GSH) and glutathione peroxidase (GPx) activity, and decreased malondialdehyde (MDA) level in the lens of diabetic rats. Luteolin also inhibited diabetes-induced elevation of interleukin-1 beta (IL-1β), vascular endothelial growth factor and nuclear factor-κB (NF-κB) mRNA and protein expression in lens. Moreover, in the high dose group (100 mg/kg), lens GSH level was decreased to normal compared to control group. The degree of oxidative and inflammatory damage was significantly reduced in luteolin-treated rats. These data suggested that luteolin can be an effective protection candidate of diabetes-induced lens neurodegeneration by inhibiting the levels of inflammatory mediators and oxidative stress.

摘要

木犀草素是一种在许多植物中富含的类黄酮,具有多种药理作用,包括抗炎、抗氧化、抗肿瘤、心脏保护和神经保护作用。目前,炎症和氧化应激已被认为是导致糖尿病性白内障发展的两个重要因素。本研究旨在探讨木犀草素对大鼠晶状体中糖尿病诱导的氧化应激和炎症的影响。通过腹腔注射 60mg/kg 的链脲佐菌素诱导糖尿病大鼠模型,然后用木犀草素 25、50 和 100mg/kg 进行 12 周的口服治疗。结果表明,木犀草素给药可增加晶状体中的抗氧化能力,如谷胱甘肽 (GSH) 和谷胱甘肽过氧化物酶 (GPx) 活性,并降低糖尿病大鼠晶状体中的丙二醛 (MDA) 水平。木犀草素还抑制了糖尿病诱导的白细胞介素-1β (IL-1β)、血管内皮生长因子和核因子-κB (NF-κB) mRNA 和蛋白在晶状体中的表达升高。此外,在高剂量组 (100mg/kg) 中,与对照组相比,晶状体 GSH 水平降低至正常水平。木犀草素治疗的大鼠中氧化和炎症损伤的程度明显降低。这些数据表明,木犀草素通过抑制炎症介质和氧化应激的水平,可能成为治疗糖尿病性晶状体神经退行性变的有效保护候选物。

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