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原花青素对链脲佐菌素诱导的糖尿病大鼠氧化应激和炎症的改善作用。

Ameliorative effects of proanthocyanidin on oxidative stress and inflammation in streptozotocin-induced diabetic rats.

作者信息

Lee Young A, Kim You Jung, Cho Eun Ju, Yokozawa Takako

机构信息

Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.

出版信息

J Agric Food Chem. 2007 Nov 14;55(23):9395-400. doi: 10.1021/jf071523u. Epub 2007 Oct 17.

DOI:10.1021/jf071523u
PMID:17939733
Abstract

Recent evidence strongly suggests that oxidative stress due to redox imbalance is causally associated with inflammatory processes and various diseases including diabetes. We examined the effects of proanthocyanidin from persimmon peel, using both oligomers and polymers, against oxidative stress with elucidation of the underlying mechanisms in streptozotocin-induced diabetic rats. The elevation of lipid peroxidation in the kidney and serum under the diabetic condition was decreased by the administration of proanthocyanidin. The suppression of reactive oxygen species generation and elevation of the reduced glutathione/oxidized glutathione ratio were observed in the groups administered proanthocyanidin. These results support the protective role of proanthocyanidin from oxidative stress induced by diabetes. Moreover, proanthocyanidin, especially its oligomeric form, affected the inflammatory process with regulation of related protein expression, inducible nitric oxide synthase, cyclooxygenase-2, and upstream regulators, nuclear factor kappaB, and inhibitor-binding protein kappaB-alpha. Proanthocyanidin ameliorated the diabetic condition by decreases of serum glucose, glycosylated protein, serum urea nitrogen, urinary protein, and renal advanced glycation endproducts. In particular, oligomeric proanthocyanidin exerted a stronger protective activity than the polymeric form. This suggests that the polymerization of proanthocyanidin has an effect on its protective effect against diabetes. The present study supports the beneficial effect of proanthocyanidin against diabetes and oxidative stress-related inflammatory processes.

摘要

近期证据有力地表明,氧化还原失衡导致的氧化应激与炎症过程及包括糖尿病在内的多种疾病存在因果关联。我们使用原花青素的低聚物和聚合物,研究了柿皮原花青素对链脲佐菌素诱导的糖尿病大鼠氧化应激的影响,并阐明了其潜在机制。给予原花青素可降低糖尿病状态下肾脏和血清中脂质过氧化的升高。在给予原花青素的组中观察到活性氧生成的抑制以及还原型谷胱甘肽/氧化型谷胱甘肽比值的升高。这些结果支持了原花青素对糖尿病诱导的氧化应激的保护作用。此外,原花青素,尤其是其低聚体形式,通过调节相关蛋白表达、诱导型一氧化氮合酶、环氧化酶 -2 以及上游调节因子核因子κB和抑制剂结合蛋白κB -α,影响炎症过程。原花青素通过降低血清葡萄糖、糖化蛋白、血清尿素氮、尿蛋白和肾脏晚期糖基化终产物改善糖尿病状态。特别是,低聚原花青素比聚合形式具有更强的保护活性。这表明原花青素的聚合对其抗糖尿病保护作用有影响。本研究支持了原花青素对糖尿病以及氧化应激相关炎症过程的有益作用。

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