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蜜瓜苷 V 通过调节肺微生物群和纠正脂多糖诱导的肺损伤中的 Th17/Treg 失调来改善肉鸡肺部炎症。

Mogroside V ameliorates broiler pulmonary inflammation via modulating lung microbiota and rectifying Th17/Treg dysregulation in lipopolysaccharides-induced lung injury.

机构信息

Research Centre for Livestock Environmental Control and Smart Production, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

Research Centre for Livestock Environmental Control and Smart Production, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

出版信息

Poult Sci. 2023 Dec;102(12):103138. doi: 10.1016/j.psj.2023.103138. Epub 2023 Sep 22.

DOI:10.1016/j.psj.2023.103138
PMID:37862871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10590742/
Abstract

The dysbiosis of lung microbiota and inflammatory factors play a crucial role in the occurrence of lipopolysaccharides (LPS)-induced lung injury. Recently, mogroside V (MGV) has received increasing attention due to its potential health benefits in pneumonia, but its complex mechanism needs further experimental elucidation. In this study, we established an LPS-induced chicken lung injury model to investigate the protective effect of MGV on LPS-induced acute lung injury in broiler and its related mechanisms. A total of 192 one-day-old white-finned broilers were randomly assigned into 4 groups with 6 replicates: 1) control group: basal diet (d 1-44), saline (d 43); 2) LPS group: basal diet (d 1-44), LPS (d 43); 3) MGV group: basal diet + 0.2% MGV (d 1-44), saline (d 43); 4) MGV-LPS group: basal diet + 0.2% MGV (d 1-44), LPS (d 43). The results showed that pathological examination showed that lung tissue inflammation infiltration was reduced after MGV treatment. In addition, MGV can promote the balance of Th17 and Treg cell cytokines, significantly inhibit the expression of proinflammatory cytokines (IL-1β (P < 0.01), IL-6 (P < 0.001), IL-17F (P < 0.05)), and decrease immunosuppressive target expression (PD-L1 (P < 0.01), PD-1 (P < 0.001), RORα (P < 0.001)), activating the immune system. Furthermore, 16S rRNA sequencing analysis showed that MGV treatment could increase the abundance of beneficial bacteria in the lung and reduce the abundance of bacteria associated with inflammation. Generally, MGV intervention has a preventive effect on the pathological damage induced by lipopolysaccharides. Its mechanism is related to inhibiting the inflammatory response, regulating the Th17/Treg balance, and maintaining the stability of lung microbiota.

摘要

肺微生物群失调和炎症因子在脂多糖(LPS)诱导的肺损伤发生中起着关键作用。最近,由于其在肺炎方面的潜在健康益处,罗汉果苷 V(MGV)受到越来越多的关注,但它的复杂机制需要进一步的实验阐明。在这项研究中,我们建立了 LPS 诱导的鸡肺损伤模型,以研究 MGV 对肉鸡 LPS 诱导的急性肺损伤的保护作用及其相关机制。将 192 只 1 日龄白羽肉鸡随机分为 4 组,每组 6 个重复:1)对照组:基础日粮(第 1-44 天),生理盐水(第 43 天);2)LPS 组:基础日粮(第 1-44 天),LPS(第 43 天);3)MGV 组:基础日粮+0.2%MGV(第 1-44 天),生理盐水(第 43 天);4)MGV-LPS 组:基础日粮+0.2%MGV(第 1-44 天),LPS(第 43 天)。结果表明,MGV 处理后,肺组织炎症浸润减少。此外,MGV 可以促进 Th17 和 Treg 细胞细胞因子的平衡,显著抑制促炎细胞因子(IL-1β(P<0.01)、IL-6(P<0.001)、IL-17F(P<0.05))的表达,并降低免疫抑制性靶基因的表达(PD-L1(P<0.01)、PD-1(P<0.001)、RORα(P<0.001)),激活免疫系统。此外,16S rRNA 测序分析表明,MGV 处理可增加肺内有益菌的丰度,减少与炎症相关的细菌丰度。总的来说,MGV 干预对脂多糖诱导的病理损伤具有预防作用。其机制与抑制炎症反应、调节 Th17/Treg 平衡和维持肺微生物群稳定性有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/37448107736a/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/a4bb667e3979/gr1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/78e742aaf2d4/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/3a30160f0653/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/f5948f0f81f8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/6adf11097a9b/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/37448107736a/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/a4bb667e3979/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/736d1cbc3f8e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/78e742aaf2d4/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/3a30160f0653/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/f5948f0f81f8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/6adf11097a9b/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8511/10590742/37448107736a/gr7.jpg

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