4.7 Article

Ginkgo biloba extract ameliorates atherosclerosis via rebalancing gut flora and microbial metabolism

期刊

PHYTOTHERAPY RESEARCH
卷 36, 期 6, 页码 2463-2480

出版社

WILEY
DOI: 10.1002/ptr.7439

关键词

atherosclerosis; Ginkgo biloba extract; gut microbiota; intestinal barrier; targeted metabolomics

资金

  1. National Natural Science Foundation of China [81720108032, 81773986, 81930109, 81973559]
  2. Overseas Expertise Introduction Project for Discipline Innovation [G20582017001]
  3. Sanming Project of Medicine in Shenzhen [SZSM201801060]
  4. State Key Laboratory of Natural Medicines, China Pharmaceutical University [SKLNMZZ202020]

向作者/读者索取更多资源

This study confirmed the beneficial effects of Ginkgo biloba leave extract (GbE) in alleviating hypercholesterolemia, inflammation, and atherosclerosis. GbE treatment reshaped the intestinal microbiota, downregulated proinflammatory cytokines, and enhanced the expression of tight junction proteins. It also reversed the dysfunction of microbial metabolic phenotypes and reduced atherosclerotic plaque areas. These findings provide important insights into the pharmacological mechanism underlying the antiatherogenic efficacy of GbE.
The Ginkgo biloba leave extract (GbE) is widely applied in the prevention and treatment of atherosclerotic cardiovascular diseases in clinical practice. However, its mechanism of actions has not been totally elucidated. In this study, we confirmed the beneficial effects of GbE in alleviating hypercholesterolemia, inflammation and atherosclerosis in Ldlr(-/-) mice, which were fed 12 weeks of Western diet (WD). Moreover, 16S rRNA sequencing revealed that GbE treatment reshaped the WD-perturbed intestinal microbiota, particularly decreased the Firmicutes/Bacteroidetes ratio and elevated the abundance of Akkermansia, Alloprevotella, Alistipes, and Parabacteroides. Furthermore, GbE treatment downregulated the intestinal transcriptional levels of proinflammatory cytokines and enhanced the expression of tight junction proteins, exerting the roles of attenuating the intestinal inflammation as well as repairing the gut barrier. Meanwhile, the targeted metabolomic analysis displayed that GbE treatment significantly reversed the dysfunction of the microbial metabolic phenotypes, including promoting the production of short chain fatty acids, indole-3-acetate and secondary bile acids, which were correlated with the atherosclerotic plaque areas. Finally, we confirmed GbE-altered gut microbiota was sufficient to alleviate atherosclerosis by fecal microbiota transplantation. In summary, our findings provide important insights into the pharmacological mechanism underlying the antiatherogenic efficacy of GbE.

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