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Pilose antler polypeptides ameliorate inflammation and oxidative stress and improves gut microbiota in updates hypoxic-ischemic injured rats

机译:pilose鹿茸多肽改善炎症和氧化应激,并改善肠道微生物酵母在缺氧缺血受伤大鼠的更新中

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Pilose antler polypeptides (PAP) have recently been found to be effective in the treatment of brain damage in hypoxic-ischemic encephalopathy (HIE). However, the impacts of hypoxic-ischemic (HI)-induced injury on oxidative stress and inflammation in peripheral tissues remain unclear. In the present study, we hypothesized that the administration of PAP might exert a protective effect on HI-induced peripheral tissue dysfunction. To that end, HI-injured rats were administered PAP for 3 weeks, and then the metabolic phenotypes and gut microbiota were evaluated by qPCR and 16S rRNA sequencing analysis. Hepatic lipid accumulation, systemic oxidative stress and inflammation, as well as impaired gut barrier function and altered gut microbiota were found in HI-injured rats, which were reversed by the treatment of PAP. PAP treatment modulated the abundance and composition of gut microbiota, and PICRUSt analyses revealed that PAP treatment also led to a functional change in the microbial communities. These protective effects of PAP were associated with attenuated susceptibility to bacterial infections, decreased antibiotic synthesis and changed cellular processes and signaling, which may cause inflammation, barrier dysfunction, oxidative stress and mitochondria dysfunction in HI rats. In conclusion, these results suggested that PAP protected against HI-induced peripheral tissue damage in rats and therefore might be a potential candidate for the treatment of HIE and its complications. (C) 2019 Elsevier Inc. All rights reserved.
机译:最近发现pilose鹿茸多肽(PAP)在治疗缺氧缺血性脑病(HIE)中的脑损伤是有效的。然而,缺氧缺血(HI)损伤对外周组织中氧化应激和炎症的影响仍不清楚。在本研究中,我们假设PAP的给药可能对Hi诱导的外周组织功能障碍产生保护作用。为此,将Hi-Wrbed大鼠施用3周,然后通过QPCR和16S rRNA测序分析评估代谢表型和肠道微生物。在Hi-Wrought大鼠中发现了肝脂肪积累,全身氧化应激和炎症,以及肠道屏障功能受损,改变的肠道微生物A,其通过治疗PAP逆转。 PAP治疗调节了肠道微生物的丰度和组成,而Picrust分析表明,PAP治疗也导致了微生物社区的功能变化。 PAP的这些保护作用与减毒对细菌感染的敏感性有关,减少抗生素合成和改变细胞过程和信号传导,这可能导致炎症,屏障功能障碍,氧化应激和大鼠线粒体功能障碍。总之,这些结果表明,PAP免受大鼠的高诱导的外周组织损伤,因此可能是治疗HIE及其并发症的潜在候选者。 (c)2019 Elsevier Inc.保留所有权利。

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