Inhibitory Effect Of APS On Cardiac Hypertrophy Induced By Abdominal Aorta Constriction In Rats

ObjectiveTo examine the protect effect and inflammatory signaling pathwaymechanisms of APS on the cardiac hypertrophy caused by abdominal aortaconstriction(AAC) in rats.MethodsThe rat left ventricular hypertrophy(LVH) model was induced by abdominalaorta coarctation(AAC). SD rats were randomly divided into five groups:thesham group,AAC group and three APS treatment groups in which the rats wereadministered with200,400and800mg/kg.Five weeks later,the tissue of heart todetect cardiac function and cardiac index.The change of morphology wasdetected by optical mirror with pathologica section by HE stain. The expressionof interleukin1β（IL-1β）and tumor necrosis factor α(TNF-α) were determinedby enzyme-linked immunosorbent assay（ELISA）The protein expression ofP65、IκBα、TLR4were determined by western-blot.The expression of Arialnatriuretic peptide(ANP) mRNA、TLR4mRNA were determined by RT-PCR.ResultsCompared with sham group,AAC group significantly decreased the cardiacfunction;increased the cardiac index and ANP mRNA expression(P<0.01).Compared with AAC group,APS treatment group （400mg/kg,800mg/kg） were able to inhibit the AAC induced cardiachypertrophy(P<0.05or P<0.01),expressed as the cardiac function increased,thecardiac index and ANP mRNA expression decreased. IL-1β、TNF-α expressionreduced. TLR4mRNA and p65TLR4protein expression decreased, IκBαexpression increased. Compared with AAC group,APS treatment group（200mg/kg）TLR4mRNA and Maximum rate of decrease of left ventricular pressureexpressed increased, others have no significant differences（P>0.05）.ConclusionAPS can protect the rat LVH and inflammatory induced by AAC，whichmay be involved in its inhibition on the TLR4/NF-κB signal pathway.