Open AccessQuercetin attenuates lipopolysaccharide-induced myocardial cell apoptosis via modulation of cAMP-Epac pathway
Author(s) -
Yuhui Wang,
Qian Fu,
Baning Ye,
Yanpei Liu
Publication year - 2021
Publication title -
tropical journal of pharmaceutical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.209
H-Index - 36
eISSN - 1596-5996
pISSN - 1596-9827
DOI - 10.4314/tjpr.v18i9.4
Subject(s) - apoptosis , lipopolysaccharide , propidium iodide , chemistry , microbiology and biotechnology , gene knockdown , programmed cell death , biology , biochemistry , immunology
Purpose: To investigate the effects and mechanism of action of quercetin (QUE) on sepsis-induced apoptosis of myocardial cells in vitro.
Methods: Lipopolysaccharide (LPS) was used to induce apoptosis H9c2 myocardial cells. Apoptosis of H9c2 cells was determined by propidium iodide staining. Knock down of Epac1 was achieved using small interfering RNA (SiEpac1). The levels of associated proteins (Epac1 and Rap1) were evaluated by western blotting.
Results: Lipopolysaccharide promoted apoptosis of H9c2 cells and inhibited the activity of cAMP-Epac pathway (p < 0.001 vs. control). Quercetin inhibited caspase 3 activity and apoptosis (p < 0.05 vs. LPS) induced by LPS via activation of cAMP-Epac1 signaling pathway. Moreover, Epac1 knockdown decreased the anti-apoptosis effect of Que, which indicates that Que attenuated apoptosis partly via cAMP-Epac pathway.
Conclusion: Que attenuated LPS-induced apoptosis in myocardial cells via activation of cAMP-Epac1 pathway. Therefore, quercetin treatment may serve as a promising strategy in the treatment of sepsisinduced myocardial injury.