4.7 Article

Ligustrum robustum (Roxb.) blume extract modulates gut microbiota and prevents metabolic syndrome in high-fat diet-fed mice

Journal

JOURNAL OF ETHNOPHARMACOLOGY
Volume 268, Issue -, Pages -

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2020.113695

Keywords

Ligustrum robustum; High-fat diet; Metabolic syndrome; Glucose intolerance; Gut microbiota

Funding

  1. National Natural Science Foundation of China [81903946, 81873098]
  2. Emergency Special Project of National Key RD Plan [2020YFC0845800]
  3. Educational Commission of Hubei Province of China [D20182002, Q20192004]
  4. Health Commission of Hubei Province of China [ZY 2019Z001]
  5. Guizhou Medical University-the State Key Laboratory of Utilization of Medicinal Plants [FAMP201705K]

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LRE, mainly composed of ligupurpuroside A and aceteoside, alleviated insulin resistance and improved hepatic metabolism in HFD-fed mice. It also reshaped the gut microbiota structure by increasing the levels of genera Streptococcus, Lactobacillus, and Mucispirillum while decreasing the populations of Alistipes and Lachnospiraceae NK4A136 group in HFD-fed mice. The altered gut microbiota was associated with several metabolic pathways of gut bacteria, indicating the potential of LRE as a gut microbial regulator for preventing metabolic syndrome.
Ethnopharmacological relevance: In Chinese folk medicine, Ligustrum robustum (Roxb.) Blume has been widely used as a healthy tea beverage for improvement in obesity and lipidemic metabolic disorders. Aim of the study: We aimed to investigate the effect of L. robustum extract (LRE) on metabolic syndrome in high fat diet (HFD)-fed mice and to explore the underlying role of gut microbiota during the treatment. Materials and methods: The ground dried leaves of L. robustum (Roxb.) Blume were extracted with ethanol and then purified by a resin column. The composition of L. robustum extract (LRE) was analyzed by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). C57BL/6 J mice fed with HFD were treated with LRE for 16 weeks. RT-qPCR and morphological staining were utilized to reveal the impact of LRE on hepatic glucolipid metabolism and gut integrity. The next-generation sequencing of 16 S rDNA was applied for analyzing the gut microbial community of fecal samples. Results: LRE, mainly composed of ligupurpuroside A and aceteoside, alleviated insulin resistance, improved hepatic metabolism, enhanced intestinal integrity, and suppressed inflammatory responses in HFD-fed mice. Moreover, LRE treatment reshaped the gut microbiota structure by increasing the levels of genera Streptococcus, Lactobacillus, and Mucispirillum and decreasing the populations of Alistipes and Lachnospiraceae NK4A136 group in HFD-fed mice. The alteration of gut microbiota was associated with several metabolic pathways of gut bacteria. Spearman's correlation analysis further confirmed the links between the changed intestinal bacteria and multiple disease indices. Conclusions: LRE prevented gut microbiota dysbiosis and metabolic disorder in HFD-fed mice, which helps to promote the application in LRE-mediated prevention from metabolic syndrome as a gut microbial regulator.

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