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评价灵芝多糖对丙烯酰胺诱导的大鼠小肠组织损伤的保护作用。

Evaluation of the protective effects of Ganoderma atrum polysaccharide on acrylamide-induced injury in small intestine tissue of rats.

机构信息

State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China.

Hefei Taksong Biotech Co., Ltd., Hefei 230022, China.

出版信息

Food Funct. 2019 Sep 1;10(9):5863-5872. doi: 10.1039/c9fo01452g. Epub 2019 Aug 29.

Abstract

This research investigated the protective effects of Ganoderma atrum polysaccharide (PSG-1) on acrylamide (AA) induced intestinal injury in rats. Our results showed that PSG-1 pretreatment effectively reduced the levels of malondialdehyde (MDA), but increased the activity of catalase (CAT), superoxide dismutase (SOD), glutathione (GSH) and the total glutathione (T-GSH), and significantly reduced oxidative stress in AA treated rats. Furthermore, PSG-1 pretreatment down-regulated pro-inflammatory cytokines i.e. interleukin 2 (IL-2), interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) and increased the amounts of anti-inflammatory cytokines i.e. interleukin 4 (IL-4) and interleukin 10 (IL-10), significantly reducing an inflammatory response in the intestines of rats. In AA induced intestinal injury, the tissue uric acid (UA) level and alkaline phosphatase (ALP) activity and the serum level of d-lactic acid (d-lactate), nitric oxide (NO) and endothelin-1 (ET-1) decreased significantly after treatment with PSG-1 and N-acetylcysteine (NAC). Histological observations of the small intestine confirmed the protective effects of different doses of PSG-1. These findings suggested that PSG-1 pretreatment could alleviate AA-induced oxidative stress, reduce inflammatory response, and inhibit AA absorption by protecting the intestinal barrier. Therefore, Ganoderma atrum polysaccharide has the potential to be a dietary supplement ingredient that provides protection against AA-induced gut injury.

摘要

本研究探讨了灵芝多糖(PSG-1)对丙烯酰胺(AA)诱导大鼠肠道损伤的保护作用。我们的结果表明,PSG-1 预处理可有效降低丙二醛(MDA)水平,提高过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)和总谷胱甘肽(T-GSH)的活性,显著减轻 AA 处理大鼠的氧化应激。此外,PSG-1 预处理可下调促炎细胞因子白细胞介素 2(IL-2)、白细胞介素 1β(IL-1β)和肿瘤坏死因子-α(TNF-α)的含量,增加抗炎细胞因子白细胞介素 4(IL-4)和白细胞介素 10(IL-10)的含量,显著减轻大鼠肠道的炎症反应。在 AA 诱导的肠道损伤中,经 PSG-1 和 N-乙酰半胱氨酸(NAC)处理后,组织尿酸(UA)水平、碱性磷酸酶(ALP)活性以及血清中二胺氧化酶(DAO)、D-乳酸(D-lactate)、一氧化氮(NO)和内皮素-1(ET-1)水平显著降低。PSG-1 不同剂量预处理对小肠的组织学观察证实了其保护作用。这些发现表明,PSG-1 预处理可通过保护肠道屏障减轻 AA 诱导的氧化应激、减少炎症反应和抑制 AA 吸收,从而发挥保护作用。因此,灵芝多糖有可能成为一种膳食补充剂成分,提供对 AA 诱导的肠道损伤的保护作用。

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