Capsaicin protects cardiomyocytes against lipopolysaccharide-induced damage via 14-3-3γ-mediated autophagy augmentation

The results showed that cardiomyocyte viability decreased, lactate dehydrogenase and creatine kinase activities increased, 14-3-3γ expression was downregulated, and autophagy was inhibited after LPS challenge

Yang Qiao; Liang Wang; Tianhong Hu; Dong Yin; Huan He; Ming He

2021

Scholarcy highlights

  • Sepsis is characterized by high mortality in intensive care units
  • The potential pathway of 14-3-3γ-dependent autophagy and the effects and mechanisms of Cap were studied in LPS-induced injury to primary cultured neonatal rat cardiomyocytes
  • The results showed that cardiomyocyte viability decreased, lactate dehydrogenase and creatine kinase activities increased, 14-3-3γ expression was downregulated, and autophagy was inhibited after LPS challenge
  • These data indicated that LPS toxicity could downregulate 14-3-3γ expression and trigger cardiomyocyte injury, but pretreatment with Cap could upregulate the 14-33γ protein and alter the cell viability plus lactate dehydrogenase and creatine phosphate kinase activities to protect cardiomyocytes
  • Active phosphorylation sites of AMP-activated protein kinase and unc-51 like autophagy-activating kinase 1, plus mammalian target of rapamycin levels were reversed by Compound C addition. These results demonstrated that Cap pretreatment involved a positive adjustment in autophagy level by upregulating 14-3-3γ, AMPK, and ULK1 levels, and suppressing mTOR expression
  • NDUFB8 and cytochrome b-c1 complex subunit 2 expression were inhibited by LPS-induced toxicity, but Cap pretreatment could promote NDUFB8 and UQCRC2 expression by upregulating 14-3-3γ levels. These findings indicated that LPS stimulated intracellular/mitochondrial reactive oxygen species by inhibiting Complex I/III activities in the cardiomyocytes, but these negative effects could be weakened by Cap pretreatment
  • Further studies are needed to explore the potential mechanism of Cap-upregulated 14-3-3γ expression, and how the AMP-activated protein kinase-mammalian target of rapamycin/unc-51 like autophagy-activating kinase 1 pathway regulates IL-1β, TNF-α, IL-6, and IL-10 in LPS-stimulated cardiotoxicity during the mitophagy process

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