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来自[具体来源未明确]的含硒多糖通过抑制肠道微生物群介导的肝脏炎症减轻镉诱导的小鼠毒性。

Selenium-containing polysaccharide from alleviates Cd-induced toxicity in mice by inhibiting liver inflammation mediated by gut microbiota.

作者信息

Zhou Ning, Long Hairong, Yu Lian, Xia Xianghua, Zhu Zhenjun, Liu Xiaoling

机构信息

College of Light Industry and Food Engineering, Guangxi University, Nanning, China.

Guangxi Botanical Garden of Medicinal Plants, Nanning, China.

出版信息

Front Nutr. 2022 Nov 3;9:950062. doi: 10.3389/fnut.2022.950062. eCollection 2022.

Abstract

Selenium-containing polysaccharide from (Se-SPP) has been demonstrated to help in inhibiting cadmium-induced injury in mice, but the underlying mechanism has not been determined. This study aimed to investigate the beneficial effects of Se-SPP on alleviating Cd-induced toxicity in mice by targeting liver inflammatory and gut microbiota. Se-SPP supplementation for 28 days in Cd-induced toxic mice significantly mitigated liver pathological damage and inflammation, which was correlated to the upregulation of antioxidant enzyme activity. Furthermore, Se-SPP effectively restored Cd-induced disruption of the intestinal barrier compared to model group, as indicated by the depletion of and the enrichment of . Spearman's correlation analysis revealed that the Se-SPP-altered microbes were highly correlated with inflammation-related indexes in Cd-induced toxic mice. Noteworthily, the modulation of Se-SPP on the population contributed to the improvement of Cd-induced inflammation-related diseases by downregulating the tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in the liver. These findings suggested that Se-SPP may act as prebiotics for ameliorating Cd-induced toxicity in mice by inhibiting liver inflammation mediated by gut microbiota, and target-specific microbiota of Cd-induced inflammation-related diseases deserve further attention.

摘要

来自[具体来源未给出]的含硒多糖(Se-SPP)已被证明有助于抑制镉诱导的小鼠损伤,但其潜在机制尚未确定。本研究旨在通过靶向肝脏炎症和肠道微生物群来探讨Se-SPP对减轻镉诱导的小鼠毒性的有益作用。在镉诱导的中毒小鼠中补充Se-SPP 28天可显著减轻肝脏病理损伤和炎症,这与抗氧化酶活性的上调相关。此外,与模型组相比,Se-SPP有效恢复了镉诱导的肠道屏障破坏,表现为[具体指标1]的减少和[具体指标2]的富集。Spearman相关性分析表明,Se-SPP改变的微生物与镉诱导的中毒小鼠的炎症相关指标高度相关。值得注意的是,Se-SPP对[具体微生物群]群体的调节通过下调肝脏中的肿瘤坏死因子-α(TNF-α)和干扰素-γ(IFN-γ),有助于改善镉诱导的炎症相关疾病。这些发现表明,Se-SPP可能作为益生元,通过抑制肠道微生物群介导的肝脏炎症来改善镉诱导的小鼠毒性,并且镉诱导的炎症相关疾病的靶向特异性微生物群值得进一步关注。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6492/9669715/94e42a4ad55f/fnut-09-950062-g0001.jpg

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