Disrupting atherosclerotic plaque formation via the "qi meridian-blood channel": mechanism of Jiangzhi Huaban Decoction for regulating hepatic reverse cholesterol transport to improve atherosclerosis.
10.12122/j.issn.1673-4254.2025.09.02
- Author:
Hongyang WANG
1
;
Wenyi ZHU
1
;
Xushen CHEN
1
;
Tong ZHANG
1
;
Zhiwei CAO
2
;
Jin WANG
2
;
Bo XIE
2
;
Qiang LIU
3
;
Xuefeng REN
1
Author Information
1. School of Public Health, Zhejiang Chinese Medical University, Hangzhou 310053, China.
2. Zhejiang Chinese Medical University-Suzhou Chongsheng Medicine Joint Laboratory, Hangzhou 310053, China.
3. Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou 310053, China.
- Publication Type:Journal Article
- Keywords:
Jiangzhi Huaban Decoction;
atherosclerosis;
qi meridian-blood channels;
reverse cholesterol transport;
vascular cell adhesion molecules
- MeSH:
Animals;
Drugs, Chinese Herbal/therapeutic use*;
Mice, Inbred C57BL;
Plaque, Atherosclerotic/metabolism*;
Liver/metabolism*;
Mice;
Atherosclerosis/metabolism*;
Cholesterol/metabolism*;
PPAR gamma/metabolism*;
Male;
Diet, High-Fat;
Biological Transport
- From:
Journal of Southern Medical University
2025;45(9):1818-1829
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To explore the molecular mechanism of Jiangzhi Huaban Decoction (JZHBD) for improving atherosclerosis through the "qi meridian-blood channels" pathway.
METHODS:ApoE-/- mouse models of atherosclerosis were established by high-fat diet feeding for 8 weeks, with C57BL/6 mice on a normal diet as the controls. Forty ApoE-/- mouse models were randomized into model group, low-, medium-, and high-dose JZHBD treatment groups, and atorvastatin treatment group (n=8) for their respective treatments for 8 weeks. The changes in body weight and overall condition of the mice were monitored weekly. After the treatments, serum levels of TC, TG, HDL-C, LDL-C, TBA, ALT, and AST of the mice were measured, pathological changes in the liver and aortic root plaques were examined with HE staining, and lipid accumulation in the liver and aortic wall was assessed using Oil Red O staining. The core molecular mechanism was studied through transcriptomics, and the expressions of the key pathway proteins were confirmed using Western blotting and immunohistochemistry.
RESULTS:Treatment with JZHBD significantly reduced blood lipid and total bile acid levels, improved liver function and hepatic steatosis, and decreased aortic lipid deposition and plaque area in the mouse models of atherosclerosis. Transcriptomic analysis suggested that the therapeutic mechanism of JZHBD involved reverse cholesterol transport, PPAR signaling, and the inflammatory pathways. In atherosclerotic mice, JZHBD treatment obviously up-regulated hepatic expressions of PPARγ, LXRα, ABCA1, ABCG1, and CYP7A1, down-regulated hepatic expressions of p-p65/p65, IL-6, IL1β in the liver, increased ABCG5 and ABCG8 expressions in the intestines, and decreased ICAM-1 and VCAM-1 expressions in the aortic plaques.
CONCLUSIONS:JZHBD improves atherosclerotic vascular damage and plaque formation possibly by regulating hepatic reverse cholesterol transport and inflammation via modulating the hepatic PPARγ/LXRα/NF-κB signaling pathway.
