Astragaloside Ⅳ Inhibits Myocardial Hypertrophy Via The TLR-4/NF-kappa B Signaling Pathway

ObjectiveTo investigate the influence of astragaloside Ⅳ （As Ⅳ） on rats model ofmyocardial hypertrophy caused by abdominal aorta coarctation（AAC） and thetheory of this inhibition is related to TLR-4/NF-kappa B signaling pathway or not.MethodsaortiThe SD rats were randomly divided into five experiment groups: shamoperation group（sham）, AAC group, AAC+As Ⅳ group (40mg·kg^-1·d^-1,As Ⅳ40), AAC+As Ⅳ group (80mg·kg^-1·d^-1, As Ⅳ80), AAC+simvastatin group (40mg·kg^-1·d^-1, simvastatin). The rats of AAC group, As Ⅳ40group, As Ⅳ80group and simvastatin group have been made surgery of abdominal aortacoarctation before treatment. These rats were detected the heart mass index（HMI） and the leftventricular mass index （LVMI）,the trans diameter of myocardialcell（TDM）. Effects of As Ⅳ on content of hydroxyproline in left ventricular tissue.Then we detected the content of TNF-α and IL-1β in serum by ELISA, mRNAlevels of atrial natriuretic peptide（ANP） and TLR-4by RT-PCR, Proteinexpression of IκB-αby Western bolotting both NF-κB p65.ResultsThe HMI, LVMI and TDM of AAC group were higher than sham group’s. Thecontent of TNF-α and IL-1β in serum, mRNA levels of ANP and TLR-4, protein expression of NF-κB, these indexes of AAC group were higher than shamgroup’s. These indexes of As Ⅳ40group were lower slightly than AAC group’sand these indexes of As Ⅳ80group were lower observably than AAC group’s.ConclusionsTNF alpha and IL-1beta inflammation factors through the IL-1-4/participate the nf-kappa B pathway mediated myocardial hypertrophy A theoryof As Ⅳ inhibit myocardial hypertrophy via theTLR-4/NF-κB signaling pathway.