Effect of Amygdalin on LPS-induced Myocardial Inflammation by Regulating HMGA1/NF-κB Signaling Pathway
Objective:To investigate the effect of amygdalin(AMG)on lipopolysaccharide(LPS)-induced myocardial inflammation and its regulatory mechanism of high mobility ATHook protein 1(HMGA1)/nuclear factor-κB(NF-κB)signaling pathway.Methods:H9c2 cardiomyocytes were divided into control group,LPS group,AMG low-dose group,AMG high-dose group,AMG high-dose+recombinant HMGA1 group(AMG high+HMGA1 group).The proliferative activity of cardiomyocytes was detected by tetramethylazolium blue(MTT).Cardiomyocyte apoptosis rate was detected by flow cytometry.The inflammatory factors interleukin(IL)-6,IL-1β and tumor necrosis factor(TNF)-α were detected by enzyme-linked immunosorbent assay(ELISA).The expressions of HMGA1/NF-κB pathway related proteins in cardiomyocytes were detected by Western Blot.Results:Compared with the control group,the survival rate of cardiomyocytes and the expression of NF-κB inhibitory protein α(IκBα)decreased in the LPS group,while the apoptosis rate,inflammatory factor IL-6,IL-1β,TNF-α content,HMGA1 protein and phosphorylation levels of NF-κB p65 and IκBα increased(P＜0.05).Compared with the LPS group,the survival rate of cardiomyocytes and the expression of IκBα protein increased in AMG dose groups,while the apoptosis rate,inflammatory factor IL-6,IL-1β,TNF-α content,HMGA1 protein and phosphorylation levels of NF-κB p65 and IκBα decreased(P＜0.05).Overexpression of HMGA1 could reverse the protective effect of AMG on cardiomyocytes(P＜0.05).Conclusion:AMG could attenuate LPS-induced myocardial inflammation by inhibiting the HMGA1/NF-κB signalling pathway.
cardiomyocytesamygdalinhigh mobility ATHook protein 1/nuclear factor-κB signaling pathwayinflammatory responseexperimental study
万方数据
维普
