A comprehensive study on the underlying mechanisms of the lipid-lowering effects of Bao Li Er Capsule in hyperlipidemia

TL;DR

This study explores how a traditional Mongolian herbal capsule lowers high cholesterol in rats by analyzing its active ingredients and biological mechanisms.

Contribution

The study reveals the potential mechanisms of Bao Li Er Capsule in treating hyperlipidemia through network pharmacology and experimental validation.

Findings

BLEC's active components, including quercetin, bind strongly to the key target PPARG.

BLEC reduces inflammation and cholesterol by modulating PPARG, IL-6, and lipid transport proteins.

Animal experiments confirm BLEC's effects on lipid metabolism and bile acid pathways.

Abstract

A traditional Mongolian formula Bao Li Er capsule (BLEC) has demonstrated excellent therapeutic effect against hyperlipidemia; however, its underlying mechanism of action remains unknown. This study aimed to investigate how BLEC lowers hyperlipidemia (HLP) in rats using network pharmacology, molecular docking, and in vivo experiments.

Active components from BLEC's 21 herbal ingredients were identified using the Traditional Chinese Medicine Systems Pharmacology Database and literature sources. Predicted targets were analyzed using DrugBank and GeneCards databases. Intersection genes were mapped to construct a protein-protein interaction (PPI) network via the STRING database. Molecular docking assessed the binding affinities between core components and key targets. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed using the DAVID database, with findings validated through animal experiments. Network pharmacology identified 268 common targets between BLEC and HLP. Among these, five core components, including quercetin, exhibited strong binding affinity with the key HLP target, PPARG. Animal studies demonstrated that BLEC significantly downregulated PPARG and IL-6 levels, reduced Apo-B100 content, and upregulated ABCA1 and ABCG1 protein expression, thereby increasing Apo-A content. BLEC also enhanced the expression of lipid transport proteins, such as LCAT, and those involved in bile acid metabolism, like CYP7A1.

These results suggest that BLEC's active components may treat HLP by modulating cholesterol metabolism and reducing inflammation and oxidative stress.

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