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破壁灵芝孢子多糖通过调节肠道菌群抑制肥胖和炎症

Suppression of obesity and inflammation by polysaccharide from sporoderm-broken spore of Ganoderma lucidum via gut microbiota regulation.

机构信息

College of Pharmaceutical Science, Zhejiang Chinese Medical University, Hangzhou, China.

College of Pharmaceutical Science, Zhejiang Chinese Medical University, Hangzhou, China.

出版信息

Carbohydr Polym. 2021 Mar 15;256:117594. doi: 10.1016/j.carbpol.2020.117594. Epub 2021 Jan 4.

DOI:10.1016/j.carbpol.2020.117594
PMID:33483079
Abstract

Ganoderma lucidum has been shown to have anti-obesity effects. However, polysaccharide extracted from the sporoderm-broken spores of Ganoderma lucidum (BSGLP) against obesity and its underlying mechanisms have never been reported. In the current study, we showed that BSGLP inhibited high-fat diet (HFD)-induced obesity, hyperlipidemia, inflammation, and fat accumulation in C57BL/6 J mice. BSGLP improved HFD-induced gut microbiota dysbiosis, maintained intestinal barrier function, increased short-chain fatty acids production and GPR43 expression, ameliorated endotoxemia, manifested by reduced serum lipopolysaccharide level, and increased ileum expression of tight junction proteins and antimicrobial peptides. Fecal microbiota transplantation study confirmed that BSGLP-induced microbiota change is responsible, at least in part, for obesity inhibition. Besides, BSGLP notably alleviated HFD-induced upregulation of TLR4/Myd88/NF-κB signaling pathway in adipose tissue. Collectively, our study showed for the first time that BSGLP might be used as a prebiotic agent to inhibit obesity and hyperlipidemia through modulating inflammation, gut microbiota, and gut barrier function.

摘要

灵芝被证明具有抗肥胖作用。然而,从灵芝破壁孢子中提取的多糖(BSGLP)对肥胖及其潜在机制从未有过报道。在本研究中,我们发现 BSGLP 可抑制高脂肪饮食(HFD)诱导的肥胖、高血脂、炎症和脂肪堆积。BSGLP 改善 HFD 诱导的肠道微生物失调,维持肠道屏障功能,增加短链脂肪酸产生和 GPR43 表达,改善内毒素血症,表现为血清脂多糖水平降低,回肠紧密连接蛋白和抗菌肽表达增加。粪便微生物移植研究证实,BSGLP 诱导的微生物变化至少部分负责抑制肥胖。此外,BSGLP 显著减轻了 HFD 诱导的脂肪组织中 TLR4/Myd88/NF-κB 信号通路的上调。综上所述,我们的研究首次表明,BSGLP 可能通过调节炎症、肠道微生物群和肠道屏障功能,作为一种益生菌制剂来抑制肥胖和高血脂。

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