Maslinic acid protects against pressure overload-induced cardiac hypertrophy in mice

Cardiac hypertrophy is characterized by myocyte hypertrophy, accumulation of cardiac collagen, and reactivation of fetal genes. Maslinic acid (MA) is a pentacyclic triterpene with abundance in olive fruit skin and possesses a number of pharmacological actions. However, its effect on pressure overloa...

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Bibliographic Details
Published in:Journal of pharmacological sciences 2018-10, Vol.138 (2), p.116-122
Main Authors: Liu, Yan-Ling, Kong, Chun-Yan, Song, Peng, Zhou, Heng, Zhao, Xing-Sheng, Tang, Qi-Zhu
Format: Article
Language:English
Subjects:
Administration, Oral
AKT
Animals
Cardiac fibrosis
Cardiac hypertrophy
Cardiomegaly - drug therapy
Cardiomegaly - etiology
Cardiomegaly - pathology
Cardiomegaly - physiopathology
Cells, Cultured
Disease Models, Animal
ERK
Fibrosis
Hemodynamics
Male
MAP Kinase Signaling System - drug effects
Maslinic acid
Mice, Inbred C57BL
Myocytes, Cardiac - pathology
Olea - chemistry
Phosphorylation - drug effects
Phytotherapy
Pressure - adverse effects
Proto-Oncogene Proteins c-akt - metabolism
Rats
Triterpenes - administration & dosage
Triterpenes - isolation & purification
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Summary:Cardiac hypertrophy is characterized by myocyte hypertrophy, accumulation of cardiac collagen, and reactivation of fetal genes. Maslinic acid (MA) is a pentacyclic triterpene with abundance in olive fruit skin and possesses a number of pharmacological actions. However, its effect on pressure overload-induced cardiac hypertrophy remains unknown. Here, we were to investigate the protective effect of MA on cardiac hypertrophy and fibrosis. C57 mice were subjected to aortic banding (AB) or sham surgery. One day after surgery, all the mice were orally given MA (20 mg/kg) or vehicle for the following four weeks. MA could protect against pressure overload-induced cardiac hypertrophy and cardiac fibrosis, as indicated by decreased heart weight/tibia length, and cardiomyocytes cell area and hypertrophic and fibrotic markers. MA treatment also improved cardiac function in mice with AB surgery, as assessed by echocardiographic and hemodynamic analysis. MA reduced phosphorylation of protein kinase B and extracellular regulated protein kinases in the hypertrophic hearts. MA could decrease cardiomyocyte hypertrophy, and inhibit the activation of AKT and ERK signaling pathway in vitro. In conclusion, we found that MA protected against cardiac hypertrophy. MA has the potential to become a therapeutic drug for cardiac hypertrophy.
ISSN:1347-8613
1347-8648
DOI:10.1016/j.jphs.2018.08.014