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

• 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
• ISSN: 1347-8613; 1347-8648
• DOI: 10.1016/j.jphs.2018.08.014

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.