# Jianpi Qutan Decoction improves hepatic lipid metabolism in atherosclerosis mice via PPARα-CPT1α pathway regulation

**Authors:** Xiaoyu Gao, Ying Hai, Dan Ma, Lisi Liu, Ying Pei, Jie Li, Wenping Wang

PMC · DOI: 10.1186/s41065-025-00580-8 · 2025-10-15

## TL;DR

This study shows that Jianpi Qutan Decoction improves liver lipid metabolism in atherosclerosis mice by regulating the PPARα-CPT1α pathway.

## Contribution

The study demonstrates a novel herbal treatment's mechanism for improving lipid metabolism in atherosclerosis via the PPARα-CPT1α pathway.

## Key findings

- JPQT reduced hepatic triglycerides, cholesterol, and inflammation in atherosclerosis mice.
- JPQT modulated fatty acid metabolism by promoting ACC phosphorylation and suppressing FAS and FFA.
- JPQT upregulated PPARα, CPT1α, and ACOX1 expression in the liver in a dose-dependent manner.

## Abstract

To investigate Jianpi Qutan Decoction (JPQT)’s effects on hepatic lipid metabolism via the PPARα-CPT1α pathway.

Eight male C57BL/6J mice served as controls; 32 ApoE-/- mice were randomized into atherosclerosis (AS), atorvastatin calcium (AC), and low/medium/high-dose JPQT groups. Prior to the intervention, therapeutic targets of JPQT were analyzed using network pharmacology to provide a theoretical basis for subsequent experiments. The AS model was induced by a 12-week high-fat diet. Hepatic triglyceride (TG) and cholesterol (TC) were measured via GPO-PAP. Glucose tolerance (GTT) and insulin tolerance (ITT) were assessed. Pro-inflammatory cytokines were analyzed by ELISA/colorimetry. Fatty acid metabolism enzymes were evaluated using kits. PPARα-CPT1α pathway mRNA and protein expression were quantified via qPCR and Western blot.

JPQT and AC reduced aortic plaque lipid deposition. JPQT significantly lowered hepatic TG/TC, blood glucose, insulin, and inflammation. It modulated fatty acid metabolism by promoting ACC phosphorylation, suppressing FAS and FFA while elevating FAβO, with dose-dependent efficacy. Additionally, JPQT upregulated PPARα, CPT1α, and ACOX1 mRNA and protein expression in the liver.

JPQT may improves lipid metabolism and reduces AS progression by activating the PPARα-CPT1α pathway, with higher doses yielding stronger effects.

The online version contains supplementary material available at 10.1186/s41065-025-00580-8.

## Linked entities

- **Genes:** PPARA (peroxisome proliferator activated receptor alpha) [NCBI Gene 5465], CPT1A (carnitine palmitoyltransferase 1A) [NCBI Gene 1374], ACOX1 (acyl-CoA oxidase 1) [NCBI Gene 51], ACACA (acetyl-CoA carboxylase alpha) [NCBI Gene 31], FAS (Fas cell surface death receptor) [NCBI Gene 355]
- **Chemicals:** atorvastatin calcium (PubChem CID 60822), triglyceride (PubChem CID 5460048), cholesterol (PubChem CID 5997), glucose (PubChem CID 5793), insulin (PubChem CID 70678557), FFA (PubChem CID 3371)
- **Diseases:** atherosclerosis (MONDO:0005311)

## Full-text entities

- **Genes:** Cpt1a (carnitine palmitoyltransferase 1a, liver) [NCBI Gene 12894] {aka C730027G07, CPTI, Cpt1}, Ppara (peroxisome proliferator activated receptor alpha) [NCBI Gene 19013] {aka 4933429D07Rik, Nr1c1, PPAR-alpha, PPARalpha, Ppar}, Acox1 (acyl-Coenzyme A oxidase 1, palmitoyl) [NCBI Gene 11430] {aka AOX, Acox, D130055E20Rik, Paox}
- **Diseases:** inflammation (MESH:D007249), AS (MESH:D050197)
- **Chemicals:** TC (MESH:D013667), AC (MESH:D000069059), Fatty acid (MESH:D005227), FFA (MESH:D005230), TG (MESH:D014280), lipid (MESH:D008055), Glucose (MESH:D005947), cholesterol (MESH:D002784), FAbetaO (-), blood glucose (MESH:D001786), ACC (MESH:C023863)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Figures

12 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12522855/full.md

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Source: https://tomesphere.com/paper/PMC12522855