Dioscin ameliorates cardiac hypertrophy through inhibition of the MAPK and Akt/GSK3β/mTOR pathways.

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.