Astragalus polysaccharides inhibites cardiomyocyte hypertrophy induced by isoproterenol via Toll-like receptor 4/nuclear factor-κB signal pathway

Objective To discuss the effects and mechanism of astragalus polysaccharides(APS)on cardiomyocyte hypertrophy induced by isoproterenol(Iso). Methods Cardiac myocytes from SD neonatal rat were primarily cultured and induced hypertrophy by Iso(10μmol/L). The effects of NF-κB's inhibitor BAY11-7082and different concentrations of APS on hypertrophic cardiomyocyte were observed. The volume of cardiomyocytes was measured by digestive isolation and computer photograph analysis system,the total protein content by coomassie brilliant blue(Bradford),the expression of tumor necrosis factorα(TNF-α)and interleukin-6(IL-6)by enzyme-linked immunosorbent assay(ELISA),the expression of atrial natriuretic peptide(ANP)mRNA and Toll-like receptor 4(TLR4) mRNA by inverse transcription polymerase chain reaction(RT-PCR),and the expression of myocardial cell P65, IκBαand TLR4protein expression by Western blot. Results Compared with the normal control group,the cardiomyocyte size,total protein content,content of TNF-αand IL-6in Iso group increased by 88.3%,55.3%,200%, 65.9%,respectively,along with the expression of ANP mRNA,TLR4mRNA,P65protein and TLR4protein, while the protein expression of IκBαdecreased. BAY11-7082and APS could inhibit the cardiomyocyte hypertrophy induced by Iso,and decrease the inflammatory response and the expression of TLR4mRNA,with that manifestation the cell volume,total protein content,expression of ANP mRNA,TNF-αand IL-6in extracellular fluid,P65and TLR4protein decreased,and IκBαprotein increased. APS had a dose-dependent inhibitory effect. Conclusion APS could inhibit cardiomyocyte hypertrophy induced by Iso,with the mechanism that may relate to TLR4/NF-κB inflammatory signaling pathway.