Sepsis-induced cardiomyopathy is a well-known cause of mortality. Recent evidence has highlighted the important role of myricetin in anti-inflammation and anti-oxidative stress. However, little is known about its effect on endotoxin-induced cardiomyopathy. We examined the effect of myricetin on lipopolysaccharide (LPS)-induced cardiomyocyte injury and the underlying mechanisms in vitro.

mRNA expression of interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha was examined via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Protein expression levels of NF-κB/p65, IκB, IL-1beta, IL-6, and TNF-alpha were assesses via Western blotting. Immunofluorescence (IF) was used to determine the nuclear translocation of p65. Commercial kits were employed to detect the level of oxidative markers and to quantify NF-κB/p65 both in the cytoplasm and the nucleus. Finally, terminal deoxy-nucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) was performed to evaluate the apoptosis of H9c2 cardiomyocytes.

The results showed that myricetin blunted the overexpression of IL-1beta, IL-6, and TNF-alpha markedly by inhibiting the NF-κB/P65 signaling pathway. Furthermore, myricetin treatment led to the downregulation of reactive oxygen species (ROS) accompanied by increased expression of superoxide dismutase and glutathione peroxidase. TUNEL-positive nuclei were rarely detected following myricetin treatment.

Our findings suggest that myricetin is a valuable protective agent against endotoxin-induced early inflammatory responses in H9c2 cardiomyocytes, which involves regulation of ROS and the IκB/NF-κb signaling pathway.