Abstract
Cardiac hypertrophy occurs in response to multiple stimuli and develops into congestive heart failure with morbidity and mortality. Dioscin exerts protective effects against tumor growth and ischemia/reperfusion injury. However, whether and how dioscin attenuates angiotensin II (AngII)-induced cardiac hypertrophy is still unknown. In the current study, we found that dioscin attenuated cardiac hypertrophy and restored the impaired cardiac function induced by AngII infusion in vivo. In addition, dioscin blocked the activation of the MAPK and Akt/GSK3β/mTOR pathways and nuclear accumulation of p-Akt1 in AngII-infused mice. In vitro, dioscin inhibited the activation of the MAPK and Akt/GSK3β/mTOR pathways and nuclear translocation of p-Akt1 and thus alleviated the hypertrophic growth. Our study demonstrated dioscin protects against AngII-induced cardiac hypertrophy via inhibition of the MAPK and Akt/GSK3β/mTOR pathways and is a potential therapeutic candidate.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
