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首页> 外文期刊>Phytotherapy research: PTR >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
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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

机译:寡聚醇,一种源自荔枝剥离的低分子量多酚,通过抑制氧化应激缺陷型丝裂蛋白激酶/核因子-Kappa B信号来抑制炎症反应衰减糖尿病诱导的胰腺损伤

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摘要

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-kappa B), NF-kappa Bp65, and NF-kappa Bp65-induced inflammatory protein such as cyclooxygenase-2, inducible nitric oxide synthase, tumor necrosis factor-alpha, 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.
机译:本研究研究了寡核苷醇,一种低分子聚酚衍生自荔枝果皮的低分子多酚,通过氧化应激诱导的炎症造成糖尿病诱导的胰腺损伤。在10或20mg / kg体重/日口服寡核苷酸酮以10天施用10天,诱导糖尿病大鼠,并将大鼠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丧失和增加的胰腺重量,并且口服寡核醇施用这些参数。此外,寡核醇的给药导致血清葡萄糖水平的显着降低和糖尿病大鼠中血清和胰岛素胰岛素和C肽水平的显着增加。寡核苷酸还显着降低了具有氧化应激生物标志物,血清和胰腺的增强水平的活性氧物质和2-硫氨基吡咯酸反应物质。寡核苷酸处理还原过表达磷酸-P38,磷酸-ERK1 / 2,核因子-Kappa B(NF-Kappa B),NF-Kappa BP65和NF-Kappa BP65诱导的炎性蛋白如环氧氧酶 - 2,诱导型一氧化氮合酶,肿瘤坏死因子 - α和白细胞介素-6。此外,寡核苷酸处理导致胰腺中显着减弱的组织学损伤。在这些结果的基础上,我们得出结论,寡核醇的抗糖尿病作用的合理机制可能是其抗氧化应激相关的抗炎作用。

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