Aim of the study
In this study, we aim to evaluate the effect of Sal D on heart failure and elucidate its underlying mechanisms. Materials and
Conclusion
In summary, Sal D can improve the heart function of SHR by inhibiting the Ras signalling pathway and activating the PI3K/AKT signalling pathway.
Methods
Using the spontaneously hypertensive rats (SHR) as a cardiac remodelling model, the cardioprotective effect of Sal D was evaluated. Employing bioinformatics analysis, the related mechanisms of Sal D treatment on heart failure were identified and validated by Western blot and polymerase chain reaction.
Results
The results showed that Sal D significantly improved cardiac function and attenuated cardiac hypertrophy. Besides, Sal D impaired mitochondrial structure and restored the energy charge of cardiomyocytes managed by angiotensin II. Bioinformatics analysis suggested that Sal D might improve heart failure by modulating the Ras and PI3K/AKT signalling pathways verified in vitro and in vivo.