Orientin prevents myocardial remodeling after MI through the PI3K/Akt signaling pathway

In the current study, the protective role of orientin in myocardial infarction (MI) and its underlying mechanism was explored. Male C57BL/6J mice were treated with anterior wall standard MI surgery and administered orientin one week later in mice for 14 days. Improved cardiac dysfunction was observed after orientin treatment detected by echocardiographic and hemodynamic evaluation. Additionally, H&E staining demonstrated an infarct size ratio and the cardiomyocyte cross-sectional area that was lower in the MI-Ori group compared with the MI-Veh group. In addition, the fibrotic area ratio was significantly lower in the MI-Ori group detected by Masson's staining. qRT-PCR analysis showed that orientin treatment remarkably decreased the expression of fibrotic and hypertrophic biomarkers. Western blot analysis showed that orientin improved cardiac dysfunction through targeting the MAPK and PI3K/Akt signaling pathways. Taken together, the results demonstrate that orientin may improve mouse left ventricular function and attenuate cardiac remodeling by inhibition of the MAPK and PI3K/Akt signaling pathway.