# Gut Microbiota and Metabolomics Insights into the Gualou-Xiebai Herb Pair for Dyslipidemia and Atherosclerosis

## TL;DR

This study explores how the GLXB herb pair reduces cholesterol and improves gut microbiota in mice with dyslipidemia and atherosclerosis.

## Contribution

The study reveals that GLXB reduces cholesterol absorption via gut microbiota metabolite butyric acid in ApoE-/- mice.

## Key findings

- GLXB herb pair increases propionic acid and butyric acid in gut microbiota of ApoE-/- mice.
- Butyric acid reduces cholesterol levels in Caco-2 cells.
- GLXB inhibits NPC1L1, ACAT2, MTP, and ApoB48 proteins via increased butyric acid.

## Abstract

As a chronic lipid driven arterial disease, dyslipidemia is one of the most critical risk factors for atherosclerosis (AS). The gut microbiota plays an important role in regulating host lipid metabolism disorders. Studies have shown that the herb "Gualou-Xiebai" (GLXB) can effectively regulate the blood lipid levels of ApoE-/- mice and inhibit blood lipid accumulation. However, it is not yet clear whether GLXB herb pair can alleviate lipid abnormalities in AS diseases by inhibiting cholesterol absorption. Meanwhile, the regulatory effect of GLXB herb pair on gut microbiota metabolites needs further research. Therefore, ApoE-/- mice were used to establish a dyslipidemia model with a HFD approach, and the contents of the cecum of the mice were collected for a gut microbiota study and to analyze how the GLXB herbal pair ameliorates dyslipidemia through the gut microbiota in ApoE-/- mice. The results showed that the GLXB herb pair can significantly increase metabolites propionic acid and butyric acid levels in the gut microbiota. In addition, cellular experiments demonstrated that butyric acid significantly reduced cholesterol levels in Caco-2 cells, and western blot results showed that the GLXB herb pair inhibited the expression of NPC1L1, ACAT2, MTP, and ApoB48 proteins by increasing the level of butyric acid. In conclusion, the GLXB herb pair exerts a therapeutic effect on dyslipidemia in ApoE-/- mice by decreasing intestinal cholesterol absorption in ApoE-/- mice by increasing the level of butyric acid, a metabolite of the gut microbiota.