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Updated: Apr 6, 2026

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
Oleanolic acid alleviated pressure overload-induced cardiac remodeling
Hai-Han Liao1,2, Nan Zhang3, Hong Feng4
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Oleanolic acid (OA) reduces cardiac hypertrophy and fibrosis in pressure overload models by inhibiting the Akt/mTOR pathway. This suggests OA may benefit patients with cardiac remodeling.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Oleanolic acid (OA) exhibits anti-inflammatory and antioxidant properties.
- Previous studies showed OA's benefits in diabetic cardiomyopathy and autoimmune myocarditis.
- The effect of OA on pressure overload-induced cardiac remodeling is largely unknown.
Purpose of the Study:
- To investigate the effects of OA on cardiac remodeling induced by pressure overload.
- To elucidate the underlying molecular mechanisms of OA's action.
- To assess OA's therapeutic potential in cardiac remodeling.
Main Methods:
- Mice underwent aortic banding (AB) surgery and were treated with OA.
- Echocardiography and hemodynamic measurements assessed cardiac function.
- Histological analysis and RT-PCR evaluated cardiac hypertrophy and fibrosis.
- In vitro studies examined OA's effects on Angiotensin II-stimulated cells.
Main Results:
- OA treatment ameliorated systolic and diastolic dysfunction post-AB.
- OA decreased mRNA expression of cardiac hypertrophy and fibrosis markers.
- Pressure overload-induced phosphorylation of Akt, mTOR, and related proteins was attenuated by OA.
- OA inhibited Angiotensin II-induced cardiomyocyte hypertrophy and fibrosis in vitro.
Conclusions:
- Oleanolic acid suppresses pressure overload-induced cardiac hypertrophy.
- OA acts partly by inhibiting the Akt/mTOR pathway.
- OA may offer therapeutic benefits for long-term pressure overload-induced cardiac remodeling.
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