Protection Of Astragalus Polysaccharide On Lipopolysaccharide-induced Myocardial Hypertrophy

ObjectiveThe aims of our study was to investigate the protective effects andmechanism of lipopolysaccharide （LPS）-induced cardiac hypertrophy byastragalus polysaccharide （APS）.Methods1-2d in vitro cultured neonatal SD rats neonatal rat cardiac myocytes after48h, Myocardial cells of neonatal rats were cultured in vitro and were dividedinto normal control groups, LPS1mg·L^-1model group, LPS+APS5,15,45mg·L^-1group, LPS+VER1μmol·L^-1group.The total protein was measured by theBradford Protein Assay Kit, The size was assayed by computer photograanalysis; ANP mRNA expression was measured by RT-PCR;tumor necrosisfactor （TNF-α） levels was determined by enzyme-linked immunosorbent assay（ELISA）;The cell viability was assessed by MTT assayusing;Fluo-3/Amfluorescent dye load cell, the laser confocal microscope measured theconcentration of intracellular calcium transient.ResultsCompared with normal control group,LPS1mg·L^-1significantly increasedthe total protein content and size of cardiomyocytes, ANP mRNA expressionwas significantly increased,the release of TNF-α protein was significantly increased,the cell viability was decreased（P<0.01）and intracellular [Ca²⁺]itransient peak increase. Compared with the LPS model group, pre-accession5,15,45mg·L^-1of APS can inhibit myocardial cell volume and total proteincontent increases, ANP mRNA expression decreased in varying degrees，whilecells of TNF-α were significantly reduced,and the cell viability increases（P<0.05）, in which APS15,45mg·L^-1group can be restored to normal levels ofthe control group（P>0.05）, APS15mg/L LPS can antagonize the normalintracellular [Ca²⁺]itransient amplitude increased role.ConclusionsAPS do has a good protective effect of cultured cardiac myocytes and itsmechanism may be related to decreased release of TNF-α and inhibiting[Ca²⁺]i.