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Updated: Feb 10, 2026

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
Published on: June 29, 2014
Astragaloside IV protects against the pathological cardiac hypertrophy in mice
Zhen-Hu Liu1, Hong-Bo Liu1, Jun Wang1
1Department of Pediatrics, Liaocheng People's Hospital, Liaocheng, Shandong 252000, China.
Insights
Astragaloside IV (AST-IV) may prevent cardiac hypertrophy by enhancing suppressor of IKKε (SIKE). This natural compound inactivates the TBK1/PI3K/AKT pathway, reducing heart enlargement, fibrosis, and dysfunction.
Area of Science:
- Cardiovascular Biology
- Pharmacology
- Molecular Medicine
Background:
- Pathologic cardiac hypertrophy can lead to heart failure, arrhythmia, and sudden death.
- Exploring molecular mechanisms and effective treatments for cardiac hypertrophy is crucial.
- Astragaloside IV (AST-IV), from Astragalus membranaceus, exhibits anti-cancer, anti-oxidative, and anti-inflammatory properties.
Purpose of the Study:
- To investigate the effects of AST-IV on cardiac hypertrophy induced by aortic banding (AB) in mice.
- To elucidate the underlying signaling pathways modulated by AST-IV in cardiac hypertrophy.
Main Methods:
- Cardiac hypertrophy was induced in mice via aortic banding (AB) surgery.
- Mice were treated with AST-IV to assess its therapeutic potential.
- Key signaling pathways, including TBK1/PI3K/AKT and the suppressor of IKKε (SIKE) pathway, were analyzed.
Main Results:
- AST-IV treatment attenuated cardiac hypertrophy, collagen accumulation, and improved cardiac function in AB-induced mice.
- AST-IV administration reduced apoptosis and inflammation in cardiac tissues.
- AST-IV was found to enhance SIKE expression, leading to the inactivation of the TBK1/PI3K/AKT signaling pathway.
Conclusions:
- AST-IV demonstrates a protective effect against pathological cardiac hypertrophy.
- Elevating SIKE expression and suppressing the TBK1/PI3K/AKT pathway are key mechanisms for AST-IV's action.
- AST-IV represents a potential therapeutic candidate for preventing cardiac hypertrophy.
Abstract:
Although pathologic hypertrophic hearts currently maintain output, sustained cardiac hypertrophy could predispose a patient to arrhythmia and sudden death, and also cause heart failure. Thus, finding effective treatment and exploring the underlying molecular mechanisms of cardiac hypertrophy is urgently necessary. Astragaloside IV (AST-IV) is the main active component, extracted from the traditional Chinese medicinal herb Astragalus membranaceus. Previous studies have indicated that AST-IV has various bioactivities, such as anti-cancer, anti-oxidative stress and anti-inflammation. In the present study, we aimed to explore the effects of AST-IV on cardiac hypertrophy induced by aortic banding (AB) surgery in mice, and to reveal the underlying signaling mechanisms. The suppressor of IKKε (SIKE) is a negative regulator of the interferon pathway, which could be enhanced by AST-IV to ameliorate pathological cardiac hypertrophy in mice through inactivating TANK-binding kinase 1 (TBK1)/PI3K/AKT signaling pathway. AST-IV attenuated cardiac hypertrophy, collagen accumulation and abnormal cardiac functions. In addition, AB-induced apoptosis and inflammation in the heart tissue samples of mice, which were attenuated by AST-IV administration through inhibiting SIKE expression levels. Together, the findings above indicated that AST-IV might be a potential candidate to prevent cardiac hypertrophy via elevating SIKE to suppress TBK1/PI3K/AKT activity.
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