https://www.selleckchem.com/products/ulixertinib-bvd-523-vrt752271.html Res, an agonist of Sirt3, may promote the protein expression of Sirt3, LC3 and Beclin1. Res inhibited the mRNA expression of ANP and BNP, and reversed the Ang II‑induced myocardial cell hypertrophy. The addition of siRNA‑Sirt3 decreased the protein expression of Sirt3, LC3 and Beclin1, increased the mRNA expression of ANP and BNP, and weakened the inhibitory effect of Res on myocardial cell hypertrophy. Res promoted the mRNA expression of MCAD, inhibited the mRNA expression of PK, and reversed the influence of Ang II on myocardial energy metabolism. siRNA‑Sirt3 intervention significantly decreased the effect of Res in eliminating abnormal myocardial energy metabolism. In conclusion, Sirt3 may inhibit Ang II‑induced myocardial hypertrophy and reverse the Ang II‑caused abnormal myocardial energy metabolism through activation of autophagy.The present study aimed to explore the effect of Saikosaponin D (SSD) and its underlying mechanism on apoptosis and autophagy in human breast cancer MDA‑MB‑231 cells. MTT assay, flow cytometry, western blotting and confocal fluorescence microscopy detection were employed. SSD, a kind of triterpenoid saponins extracted from Radix bupleuri, has been demonstrated to have the effects of anti‑inflammatory, antioxidative and anticancer effects and can regulate autophagy. The present study revealed that SSD induced apoptosis through the activation of the p38 mitogen‑activated protein kinase (MAPK) signaling pathway in human breast cancer MDA‑MB‑231 cells. The administration of SSD promoted the phosphorylation/activation of p38 MAPK in MDA‑MB‑231 cells, whereas pretreatment with SB203580, an effective p38 MAPK inhibitor, attenuated SSD‑mediated apoptosis, the cleavage of PARP and the activation of caspase‑3. In addition, SSD blocked autophagic degradation by inhibiting autolysosome formation, resulting in the accumulation of autophagosomes. Mechanistically, the results of