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Yangxin Tongluo Decoction Protects Against Sepsis-Associated Cardiac Dysfunction Through Regulating Nrf2 Pathway
Hainan Yang1, Beijing Wu2, Die Huang3
1Department of Critical Care Medicine, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, 358 Datong Road Pudong New District, Shanghai 200137, China, shutcm.edu.cn.
Mediators of Inflammation
|July 23, 2026
Summary
Yangxin Tongluo decoction (YXTLD) protects against sepsis-induced cardiac dysfunction by reducing inflammation, oxidative stress, and apoptosis. This traditional Chinese medicine activates the Nrf2 signaling pathway, offering a potential therapeutic strategy for sepsis patients.
Area of Science:
- Cardiovascular Research
- Traditional Chinese Medicine
- Molecular Biology
Background:
- Sepsis-induced cardiac dysfunction is a leading cause of mortality in critically ill patients.
- Yangxin Tongluo decoction (YXTLD), a traditional Chinese medicine (TCM) formula, is used clinically for sepsis, but its mechanisms are not fully understood.
- This study aimed to elucidate the protective effects of YXTLD against sepsis-associated cardiac dysfunction and its underlying mechanisms involving the Nrf2 signaling pathway.
Purpose of the Study:
- To investigate the protective role of YXTLD in a mouse model of sepsis-induced cardiac dysfunction.
- To explore the effects of YXTLD on inflammation, oxidative stress, and apoptosis in cardiomyocytes.
- To determine the involvement of the Nrf2 signaling pathway in YXTLD's cardioprotective effects.
Main Methods:
- Sepsis was induced in mice using lipopolysaccharide (LPS) injection; cardiac function was assessed via echocardiography and serum biomarkers.
- LPS-stimulated H9c2 cardiomyocytes were treated with YXTLD to evaluate cell viability, inflammation (IL-1β, IL-6, TNF-α), oxidative stress (ROS, MDA, CAT, GSH), and apoptosis.
- Western blotting was used to examine the activation of the Nrf2 signaling pathway and its downstream targets (HO-1, NQO1, GCLM).
Main Results:
- YXTLD significantly improved cardiac function (ejection fraction, fractional shortening) and reduced myocardial injury markers (CK, LDH) in septic mice.
- In vitro, YXTLD dose-dependently enhanced H9c2 cell viability, suppressed pro-inflammatory cytokines, reduced reactive oxygen species (ROS) and lipid peroxidation, and inhibited apoptosis.
- YXTLD activated the Nrf2 pathway, increasing nuclear Nrf2 translocation and upregulating antioxidant proteins (HO-1, NQO1, GCLM), while restoring antioxidant levels (CAT, GSH) and reducing MDA.
Conclusions:
- YXTLD demonstrates significant cardioprotective effects against sepsis-induced cardiac dysfunction.
- These protective effects are mediated by the attenuation of inflammation, oxidative stress, and apoptosis.
- Activation of the Nrf2 signaling pathway is a key mechanism underlying YXTLD's therapeutic benefits, supporting its potential as a treatment for sepsis-associated cardiac dysfunction.