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Updated: Jan 27, 2026

Author Spotlight: Investigating HR-Dependent Cardiac Function in Mouse Models Through a Novel Atrial-Pacing Approach
Published on: July 21, 2023
Astragaloside IV alleviates heart failure by promoting angiogenesis through the JAK-STAT3 pathway
Yan-Bo Sui1, Yu Wang2, Li Liu1
1a First Unit of Department of Cardiology , First Affiliated Hospital of Heilongjiang University of Chinese Medicine , Harbin , China.
Insights
Astragaloside IV (ASI) treatment improved heart function and survival in a rat model of heart failure (HF). ASI promoted angiogenesis via the JAK-STAT3 pathway, offering new strategies for HF prevention.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Heart failure (HF) is a significant global health concern.
- Astragaloside IV (ASI), a compound from Astragalus, is used in China for cardiovascular diseases.
Purpose of the Study:
- To assess ASI's protective effects on HF in a rat model.
- To investigate ASI's role in angiogenesis-related mechanisms in HF.
Main Methods:
- Induced HF in Sprague-Dawley rats via left coronary artery ligation.
- Administered vehicle or ASI (0.1–1 mg/kg/day) orally for 6 weeks.
- Evaluated cardiac function, infarct size, vascular density, and molecular pathways (JAK-STAT3, VEGF).
Main Results:
- ASI improved rat body weight, survival rates, and cardiac function (ejection fraction, fractional shortening).
- ASI reduced infarct size by 47% and promoted angiogenesis, increasing vascular density and VEGF/CD31 expression.
- ASI activated the JAK-STAT3 pathway, enhancing VEGF promoter activity.
Conclusions:
- ASI alleviates heart failure by promoting angiogenesis through the JAK-STAT3 pathway.
- ASI presents a potential therapeutic strategy for preventing heart failure.
Context:
Heart failure (HF) is one of the most serious diseases worldwide. Astragaloside IV (ASI) is widely used for the treatment of cardiovascular disease in China.
Objective:
To evaluate the protective effect of ASI on the HF in a Sprague-Dawley rat model of left coronary artery ligation, and investigate the angiogenesis-related mechanisms.
Materials And Methods:
Left coronary artery was ligated to induce a rat model of HF, and the rats were treated with vehicle (saline) or different doses of ASI (0.1, 0.3 and 1 mg/kg/day) by oral gavage for 6 weeks. Cardiac function was evaluated by echocardiography. Infarct size was determined by triphenyltetrazolium chloride staining. Cardiac vascular density was analyzed by microangiography. Real-time PCR, Western blot and chromatin immunoprecipitation were performed to investigate the mechanisms.
Results:
ASI treatment improved the body weight and survival rate of HF rats, as well as the cardiac function of HF rats, with significantly improved ejection fraction (75.27 ± 5.75% vs. 36.26 ± 4.14%) and fractional shortening (45.39 ± 3.66% vs. 17.88 ± 1.32%). ASI reduced the infarct size of the HF rats by 47%. ASI promoted angiogenesis, with increased vascular density (2.08-fold) and induced mRNA expression of CD31 (1.81-fold) and VEGF (2.70-fold) in the ischemic heart. Furthermore, ASI induced the phosphorylation of JAK (1.89-fold) and STAT3 (2.95-fold), as well as the activity of VEGF promoter which was regulated by STAT3.
Discussion And Conclusions:
ASI alleviated HF by promoting angiogenesis through JAK-STAT3 pathway, providing novel alternative strategies to prevent HF in the future.
Related Concept Videos
The JAK-STAT Signaling Pathway
Heart Failure IV: Classification and Diagnostic Evaluation
Pathophysiology of Heart Failure
Heart Failure I: Introduction
Heart Failure II: Pathophysiology
Acute Respiratory Failure-IV

