Related Experiment Video
Updated: Jul 12, 2025

Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
Published on: November 10, 2017
Shenlian extract improves atherosclerosis by relieving adventitial inflammation.
Shuxian Han1, Chunxia Nie1, Chunmiao Wang1
1Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China.
Shenlian (SL) extract effectively treats atherosclerosis by reducing adventitial inflammation. This Chinese medicine inhibits vascular adventitial fibroblast and smooth muscle cell changes, offering a novel therapeutic approach for atherosclerosis.
Area of Science:
- Cardiovascular Research
- Inflammation Biology
- Pharmacology
Background:
- Shenlian (SL) extract, derived from Salvia miltiorrhizae and Andrographis paniculata, targets inflammation in atherosclerosis.
- Existing research links the anti-atherosclerotic effects of SL components to inflammation, but adventitial inflammation's role remains understudied.
- This study investigates SL extract's potential to mitigate atherosclerosis by addressing adventitial inflammation.
Purpose of the Study:
- To elucidate the role of adventitial inflammation in atherosclerosis progression.
- To determine if Shenlian (SL) extract can reverse atherosclerosis development mediated by adventitial inflammation.
Main Methods:
- A novel mouse model of atherosclerosis was created using LPS-soaked threads on the carotid artery in ApoE-/- mice.
- Dynamic evaluation of vascular adventitial fibroblast (VAF) phenotype, proliferation, and collagen synthesis was performed at weeks 2, 4, and 12.
- In vitro studies assessed VAF responses to LPS and co-culture effects on vascular smooth muscle cells (VSMCs).
Main Results:
- SL extract significantly reduced lipid content, adventitial inflammation, and plaque formation in the atherosclerosis model.
- SL extract reversed LPS-induced VAF phenotypic transformation, proliferation, migration, and inflammatory secretion in vivo and in vitro.
- SL extract suppressed VSMC phenotypic transformation and migration, likely via the JAK2-STAT3-MMP2 pathway.
Conclusions:
- Adventitial inflammation acts as an 'outside-in' signal, accelerating atherosclerotic plaque formation and vascular lesion severity.
- SL extract ameliorates atherosclerosis by alleviating adventitial inflammation.
- The therapeutic mechanism involves inhibiting VAF and VSMC phenotypic transformation, proliferation, and migration.
More Related Videos
Related Concept Videos
Atherosclerosis III: Management
Atherosclerosis I: Introduction
Atherosclerosis IV: Nursing Management
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests
Inflammation
Peripheral Artery Disease III: Interprofessional Care

