Effects Of Astragalus Polysaccharide On Cardiac Hypertrophy Induced By Isoproterenol Involves Tlr4/nf-kb Signaling Pathway In Rats

ObjectiveTo observe the mechanism of TLR4/NF-κB inflammation signaling pathwayon Astragalus polysaccharide (APS) inhibits myocardial hypertrophy induced byisoproterenol (ISO).MethodsThe ISO (5mg﹒kg-1﹒d-1) were used as myocardial hypertrophy modelsby intraperitoneal injection. Sixty SD rats were randomly assigned to followingsix groups(10rats for each group):the control；ISO group；ISO plus APS200mg﹒kg-1﹒d-1；ISO plus APS400mg﹒kg-1﹒d-1；ISO plus APS800mg﹒kg-1﹒d-1；ISO plus Propranolol40mg﹒kg-1﹒d-1. Administered groups wereintraperitoneal injected for3weeks, and ISO were intraperitoneal injected for2weeks in the day after that. After administration of3weeks，heart mass index(HMI) and left ventricular mass index (LVMI) of rats in each group weremeasured, and pathological section by HE staining. The expression of ANP andTLR4mRNA were observed by RT-PCR. The expression of TLR4、 p65andIκBα in the tissue were measured by Western blot, and the expression of TNF-αand IL-6were quantified by ELISA.ResultsCompared with the control, the HMI and LVMI, ANP and TLR4mRNA, theprotein expression of TLR4, p65and TNF-α, IL-6were increased, and theexpression of IκBα were decreased in ISO group(P<0.01). Compared with ISO group, APS400,800and Propranolol40mg﹒kg-1﹒d-1decreased HMI andLVMI, and could remarkably down-regulate the overexpression of ANP mRNA,TLR4mRNA, TLR4, p65and TNF-α, IL-6, and increased the expression ofIκBα(P<0.01). APS200mg﹒kg-1﹒d-1could decreased ANP mRNA, TLR4mRNA, TLR4, p65and TNF-α expression (P<0.05, P<0.01), and increased theexpression of IκBα(P<0.05).ConclusionsAPS has a protective effect on ISO-induced cardiac hypertrophy, which ispartially via inhibiting the TLR4/NF-κB signaling pathway.