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Polysaccharides from Opuntia milpa alta alleviate alloxan-induced INS-1 cells apoptosis via reducing oxidative stress and upregulating Nrf2 expression

机译:来自Ipuntia Milpa Alta的多糖可通过降低氧化应激和上调NRF2表达来缓解阿萨妥诱导的INS-1细胞凋亡

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摘要

The incidence and progression of type 2 diabetes are closely related to pancreatic beta-cell damage. Oxidative stress may be one of the key factors contributing to beta-cell apoptosis. Opuntia milpa aka polysaccharides (MAPs) are water-soluble macromolecular polysaccharides that have antidiabetic effects in vivo. Therefore, we hypothesized that MAPs might effectively prevent beta-cell apoptosis via the inhibition of oxidative damages. In this study, INS-1 cells were exposed to alloxan with different concentrations of MAPs in vitro, and the cell viability, oxidative enzyme activities, nitric oxide production, reactive oxygen species production, apoptosis, and the expression of proteins in the antioxidant nucleus transcription factor NF-E2-related factor 2 (Nrf2) pathway and proteins related to apoptosis were measured to assess oxidative stress responses and apoptosis. The results indicated that INS-1 cell viabilities and superoxide dismutase and reduced glutathione activities were significantly restored, whereas lactate dehydrogenase releases and reactive oxygen species, nitric oxide, and malondialdehyde levels were greatly decreased after MAPs treatment. We found that MAPs could attenuate alloxan-induced apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Bax and the activities of caspase-3 and caspase-9. The results of Western blot revealed that MAPs suppressed the expression of cleaved caspase-3 and cleaved PARP and upregulated the expression of nucleus Nrf2 and its downstream protein. These findings indicated that MAPs could alleviate alloxan-induced beta-cell apoptosis by reducing oxidative stress and upregulating Nrf2 expression. (C) 2020 Elsevier Inc. All rights reserved.
机译:2型糖尿病的发病率和进展与胰腺β细胞损伤密切相关。氧化应激可能是有助于β细胞凋亡的关键因素之一。 Ipuntia milpa又名多糖(地图)是水溶性大分子多糖,具有体内抗糖尿病作用。因此,我们假设地图可以通过抑制氧化损伤有效预防β细胞凋亡。在本研究中,将INS-1细胞暴露于体外不同浓度的地图,以及细胞活力,氧化酶活性,一氧化氮产生,反应性氧物种生产,细胞凋亡和蛋白质中的抗氧化核转录中的表达测量因子NF-E2相关因子2(NRF2)途径和与细胞凋亡相关的蛋白质,以评估氧化应激反应和凋亡。结果表明,INS-1细胞活性和超氧化物歧化酶和降低的谷胱甘肽活性明显恢复,而乳酸脱氢酶释放和反应性氧物种,在地图治疗后大大降低了大大降低。我们发现地图可以通过增加Bcl-2的表达和降低Bax的表达和Caspase-3和Caspase-9的活性来衰减阿昔班诱导的细胞凋亡。 Western印迹的结果显示,图抑制了切割的Caspase-3的表达并裂解PARP并上调了核NRF2及其下游蛋白的表达。这些发现表明,通过减少氧化应激和上调NRF 2表达,地图可以缓解阿昔班诱导的β细胞凋亡。 (c)2020 Elsevier Inc.保留所有权利。

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  • 来源
    《Nutrition Research》 |2020年第1期|共11页
  • 作者单位

    Jianghan Univ Wuhan Inst Biomed Sci 8 Sanjiaohu Rd Wuhan 430056 Hubei Peoples R China;

    Jianghan Univ Wuhan Inst Biomed Sci 8 Sanjiaohu Rd Wuhan 430056 Hubei Peoples R China;

    Jianghan Univ Wuhan Inst Biomed Sci 8 Sanjiaohu Rd Wuhan 430056 Hubei Peoples R China;

    Jianghan Univ Wuhan Inst Biomed Sci 8 Sanjiaohu Rd Wuhan 430056 Hubei Peoples R China;

    Jianghan Univ Wuhan Inst Biomed Sci 8 Sanjiaohu Rd Wuhan 430056 Hubei Peoples R China;

    Jianghan Univ Wuhan Inst Biomed Sci 8 Sanjiaohu Rd Wuhan 430056 Hubei Peoples R China;

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  • 正文语种 eng
  • 中图分类 营养学;
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