Astragalus Polysaccharide Attenuates Lipopolysccharide-induced Rat Cardiomyocytes Hypertrophy By Inhibition Of The TLR4/NF-κB Signaling Pathway

ObjectiveTo explore the mechanisms of astragalus polysaccharide (APS) affectinglipopolysaccharide（LPS）-induced rat cardiac myocytes hypertrophy from theaspect of TLR4-NF-κB signaling pathway.MethodsThe primary cardiac myocytes of SD rats were cultured and inducedhypertrophy by1mg/L LPS, and then treated by different concentration ofAPS(25mg/L、50mg/L、100mg/L) and IκBα phosphorylation inhibitor(BAY11-7082). Actin filaments were visualized using Rhodamine phalloidin byconfocal microscopy; and cardiac hypertrophy was assayed by thecardiomyocytes volume and the total protein content measured by computerphotograph analysis system and the method of Bradford, respectively. therelative expression level of TLR4, IκBα, p65, TNF-α and IL-1β were determinedby RT-PCR, Western blot or ELISA,ResultsLPS can singnifcantly induce cardiomyocyte hypertrophy measured byincreasing the total protein content and enlarged the size of cardiomyocytes.APS and BYA11-7082can attenuate the LPS-induced cardiac hypertrophy examined by cardiomyocytes protein content and volume; APS andBAY11-7082can also abolish the inflammatory response induced by LPS in adose-dependent manner by inhibiting the TLR4, upregulating TNF-α and IL-1βexpression, which is partially via attenuating IκBα and TNF-α signal pathway.ConclusionsAPS has a protective effect on LPS-induced cardiac hypertrophy, which ispartially via attenuating inflammatory through TLR4/NF-κB signaling pathway.