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低分子多酚 Oligonol 来源于荔枝果皮,通过氧化应激依赖性有丝分裂原激活蛋白激酶/核因子-κB 信号通路抑制炎症反应,从而减轻糖尿病引起的胰腺损伤。

Oligonol, a low-molecular-weight polyphenol derived from lychee peel, attenuates diabetes-induced pancreatic damage by inhibiting inflammatory responses via oxidative stress-dependent mitogen-activated protein kinase/nuclear factor-kappa B signaling.

机构信息

Department of Medicinal Crop Research, National Institute of Horticultural and Herbal Science, Rural Development Administration, Eumseong, Republic of Korea.

Department of Agricultural Engineering, National Institute of Agricultural Sciences, Rural Development Administration, Jeonju, Republic of Korea.

出版信息

Phytother Res. 2018 Dec;32(12):2541-2550. doi: 10.1002/ptr.6194. Epub 2018 Oct 2.

DOI:10.1002/ptr.6194
PMID:30280446
Abstract

This study investigated the effects of oligonol, a low-molecular-polyphenol derived from lychee peel, against diabetes-induced pancreatic damage via oxidative stress-induced inflammation. Oligonol was orally administered at 10 or 20 mg/kg body weight/day for 10 days to streptozotocin-induced diabetic rats, and the rats were compared with nondiabetic and diabetic control rats. The diabetic rats showed loss of body weight and increased pancreatic weight, and the oral administration of oligonol attenuated these parameters. Moreover, the administration of oligonol caused a significant decrease in the serum glucose level and a significant increase in the serum and pancreatic insulin and C-peptide levels in the diabetic rats. Oligonol also significantly reduced the enhanced levels of reactive oxygen species and 2-thiobarbituric acid reactive substance, which are oxidative stress biomarkers, in the serum and pancreas. Oligonol treatment reduced the overexpression of phospho-p38, phospho-ERK1/2, phospho-inhibitor of nuclear factor-kappa B (NF-κB), NF-κBp65, and NF-κBp65-induced inflammatory protein such as cyclooxygenase-2, inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin-6. Furthermore, oligonol treatment led to significantly attenuated histological damage in the pancreas. On the basis of these results, we conclude that a plausible mechanism of oligonol's antidiabetic action may be its antioxidative stress-related anti-inflammatory action.

摘要

本研究旨在探讨低分子多酚荔枝多酚(oligonol)通过氧化应激诱导的炎症对糖尿病诱导的胰腺损伤的影响。Oligonol 以 10 或 20mg/kg 体重/天的剂量经口给予链脲佐菌素诱导的糖尿病大鼠 10 天,并与非糖尿病和糖尿病对照大鼠进行比较。糖尿病大鼠表现出体重减轻和胰腺重量增加,而 oligonol 的口服给药可减弱这些参数。此外,oligonol 给药可使糖尿病大鼠的血清葡萄糖水平显著降低,血清和胰腺胰岛素和 C 肽水平显著升高。Oligonol 还显著降低了血清和胰腺中氧化应激生物标志物活性氧和 2-硫代巴比妥酸反应物质的升高水平。Oligonol 处理可降低磷酸化 p38、磷酸化 ERK1/2、核因子-κB(NF-κB)抑制剂磷酸化、NF-κBp65 和 NF-κBp65 诱导的炎症蛋白如环加氧酶-2、诱导型一氧化氮合酶、肿瘤坏死因子-α和白细胞介素-6 的过度表达。此外,oligonol 处理可导致胰腺的组织损伤明显减轻。基于这些结果,我们得出结论,oligonol 的抗糖尿病作用的一个合理机制可能与其抗氧化应激相关的抗炎作用有关。

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