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Ginsenoside F2-Mediated Intestinal Microbiota and Its Metabolite Propionic Acid Positively Impact the Gut–Skin Axis in Atopic Dermatitis Mice
Journal of Agricultural and Food Chemistry ( IF 6.1 ) Pub Date : 2023-12-27 , DOI: 10.1021/acs.jafc.3c06015
Dongxu Li 1 , Zhao-Bo Luo 2 , Jun Zhu 1 , Jun-Xia Wang 3 , Zheng-Yun Jin 3 , Shaobo Qi 2 , Meiling Jin 4 , Lin-Hu Quan 2
Affiliation  

Atopic dermatitis (AD) is a complex inflammatory skin disease induced by multiple factors. AD can also cause intestinal inflammation and disorders of the gut microbiota. Ginseng is a kind of edible and medicinal plant; its main active components are ginsenosides. Ginsenosides have a variety of anti-inflammatory effects and regulate the gut microbiota; however, their role in AD and the underlying mechanisms are unclear. In this study, we found that intragastric administration of ginsenoside F2 improved AD-like skin symptoms and reduced inflammatory cell infiltration, serum immunoglobulin E levels, and mRNA expression of inflammatory cytokines in AD mice. 16s rRNA sequencing analysis showed that ginsenoside F2 altered the intestinal microbiota structure and enriched the short-chain fatty acid-producing microbiota in AD mice. Metabolomic analysis revealed that ginsenoside F2 significantly increased the propionic acid (Pa) content of feces and serum in AD mice, which was positively correlated with significant enrichment of Parabacteroides goldsteinii and Lactobacillus plantarum in the intestines. Pa inhibits inflammatory responses in the gut and skin of AD mice through the G-protein-coupled receptor43/NF-κB pathway, thereby improving skin AD symptoms. These results revealed, for the first time, the mechanism by which ginsenoside F2 improves AD through the Pa (a metabolite of intestinal microbiota)–gut–skin axis.

中文翻译:

人参皂苷 F2 介导的肠道微生物群及其代谢物丙酸对特应性皮炎小鼠的肠-皮肤轴产生积极影响

特应性皮炎(AD)是一种由多种因素诱发的复杂炎症性皮肤病。AD 还会引起肠道炎症和肠道微生物群紊乱。人参是一种食、药用植物;其主要活性成分是人参皂甙。人参皂苷具有多种抗炎作用并调节肠道菌群;然而,它们在 AD 中的作用及其潜在机制尚不清楚。在本研究中,我们发现灌胃人参皂苷 F2 可改善 AD 小鼠的 AD 样皮肤症状,并减少炎症细胞浸润、血清免疫球蛋白 E 水平和炎症细胞因子 mRNA 表达。16s rRNA测序分析表明,人参皂苷F2改变了AD小鼠的肠道微生物群结构,丰富了产生短链脂肪酸的微生物群。代谢组学分析显示,人参皂苷F2显着增加AD小鼠粪便和血清中的丙酸(Pa)含量,这与肠道内金氏副杆菌植物乳杆菌的显着富集呈正相关。Pa通过G蛋白偶联受体43/NF-κB通路抑制AD小鼠肠道和皮肤的炎症反应,从而改善皮肤AD症状。这些结果首次揭示了人参皂苷 F2 通过 Pa(肠道微生物群的代谢产物)-肠-皮肤轴改善 AD 的机制。
更新日期:2023-12-27
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