Electroacupuncture Inhibits Atherosclerosis through Regulating Intestinal Flora and Host Metabolites in Rabbit

الملخص EN

Background and Objective.

As a recommended option for 43 diseases by the World Health Organization, electroacupuncture is also being used to treat some others in China.

Diet-related intestinal flora imbalance can induce atherosclerosis.

This study aims to evaluate how electroacupuncture copes with atherosclerosis through regulating intestinal flora.

Methods.

In this study, general rabbit conditions, vascular histology, metabolites, and intestinal flora structures were analyzed.

Integrated analysis of metabolomics and 16S rRNA sequencing were performed.

All the rabbits were randomly divided into four groups.

The rabbit model of atherosclerosis was established.

The histopathological change in the common carotid artery was assessed by HE staining and the structural change in the flora by 16S rRNA sequencing.

HPLC-TOF-MS and Agilent MPP 12.1 were integrated to identify and screen out differential metabolites.

Correlational analyses of every differential metabolite with intestinal flora were integrated on Omicshare platform.

Results.

Atherosclerotic rabbits showed obvious changes in general conditions, significant fibrous cap and necrotic center on carotid artery, abnormal intestinal bacteria structure, and metabolites levels.

Electroacupuncture improved the conditions, reduced lipid deposition on the carotid artery wall, diversified intestinal flora, and normalized host metabolism.

Integrated analysis showed that 149 altered metabolites were related to 22 intestinal flora, among which eight intestinal floras and 21 metabolites have relationships with atherosclerosis.

Conclusion.

Electroacupuncture can effectively reverse atherosclerosis through manipulating the structural feature of intestinal flora to influence the host metabolites.

The possible mechanisms involved activating signal pathways through host metabolites or affecting the activity of cardiovascular-related enzymes, or regulating host lipid metabolism directly.