Here, we used the LPS-induced sepsis model in neonatal rat cardiomyocytes (NRCMs), to explore (1) the role of Cap during 14-3-3γ-related autophagy process via the AMPK-mTOR/ULK1 pathway in LPS-challenged cardiomyocytes; (2) the effects of Cap in LPS-induced cardiotoxicity via regulating inflammatory cytokine release, oxidative stress, and mitochondrial dysfunction. This evidence concerns the gene MTOR and Sepsis.