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虎杖苷通过其抗氧化活性减轻胰腺β细胞损伤。

Polydatin mitigates pancreatic β-cell damage through its antioxidant activity.

机构信息

Molecular Physiology Division, Faculty of Science, Beni-Suef University, Egypt; Department of Comparative and Experimental Medicine, Nagoya City University Graduate School of Medical Sciences, Japan.

Department of Comparative and Experimental Medicine, Nagoya City University Graduate School of Medical Sciences, Japan; Department of Animal Genetic Resources, National Gene Bank, Giza, Egypt.

出版信息

Biomed Pharmacother. 2021 Jan;133:111027. doi: 10.1016/j.biopha.2020.111027. Epub 2020 Nov 26.

DOI:10.1016/j.biopha.2020.111027
PMID:33249283
Abstract

Several reports have been shown the pivotal role of oxidative stress in the progression of diabetes mellitus and its complications. Polydatin (PD), a natural phytochemical, has wide range of pharmacological actions, however, the underlying beneficial effects in pancreas was not clarified. In the current study, using in vivo and in vitro models, we investigated the possible protective effects of PD against oxidative damage in pancreatic β-cells. Diabetic rats were examined after oral administration with PD (50 mg/kg b.wt.) for 28 days. Results revealed that PD significantly enhanced glucose tolerance and insulin secretion in the bloodstream of diabetic rats as well as lipid metabolism. Interestingly, in vivo results indicated that PD decreased the lipid peroxidation, improved the antioxidant status, and inhibited the inflammation in pancreas. Alongside, we artificially induced oxidative stress by exposing the insulin-producing RINm5F cells to hydrogen peroxide in the presence or absence of PD. The co-treatment with PD preserved cell viability, reduced ROS accumulation, as well as enhanced the anti-oxidant, anti-apoptotic, and cell function markers. To conclude, PD exhibited potential action in preserving β-cell function and inhibiting oxidative damage probably through its antioxidant properties. Thus, PD could be a possible therapeutic agent for diabetic patients.

摘要

已有多项报告表明,氧化应激在糖尿病及其并发症的发展过程中起着关键作用。虎杖苷(PD)是一种天然植物化学物质,具有广泛的药理作用,但它对胰腺的潜在有益作用尚未阐明。在本研究中,我们使用体内和体外模型,研究了 PD 对胰腺β细胞氧化损伤的可能保护作用。糖尿病大鼠给予 PD(50mg/kg 体重)口服 28 天后进行检查。结果表明,PD 可显著增强糖尿病大鼠血液中的葡萄糖耐量和胰岛素分泌,以及改善脂代谢。有趣的是,体内结果表明 PD 可降低脂质过氧化,改善抗氧化状态,并抑制胰腺炎症。此外,我们通过在存在或不存在 PD 的情况下将胰岛素产生的 RINm5F 细胞暴露于过氧化氢来人为诱导氧化应激。PD 的共同治疗可保持细胞活力,减少 ROS 积累,并增强抗氧化、抗凋亡和细胞功能标志物。总之,PD 通过其抗氧化特性表现出保护β细胞功能和抑制氧化损伤的潜在作用。因此,PD 可能是糖尿病患者的一种潜在治疗药物。

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