Effect of STAT3 in mechanism of fuzi polysaccharides postconditioning protecting cardiomyocytes with hypoxia-reoxygenation in neonate rats

Objective To investigate the protective mechanism of fuzi polysaccharides(FPS)postconditioning to cardiomyocytes with hypoxia-reoxygenation(H/R)taking signal transducers and activators of transcription 3(STAT3)as entry point.Methods The model of cardiomyocytes with H/R was established in neonate rats and then divided into normal group,H/R group,FPS group,Stattic(specific blocker of STAT3)and FPS group(Stattic+FPS group)and Stattic group.The apoptosis rate of myocardiocytes was detected by using flow cytometer,expressions of phosphorylation STAT3(P-STAT3),cytochrome C(CytC)and caspase-3 were detected by applying Western blotting and expressions of Bcl-xl mRNA and Bcl-xs mRNA were detected by using fluosescence quantitative PCR.Results FPS postconditioning improved P-STAT3 expression,up-regulated Bcl-xl mRNA expression and down-regulated Bcl-xs mRNA expression,blocked the release of CytC and caspase-3 expression,and inhibited myocardiocyte apoptosis.Stattic can reverse the protective effect of FPS to cardiomyocytes and increase of P-STAT3 expression.Conclusion The protective effect of FPS to cardiomyocytes with H/R is related to the activation of STAT3,increase of Bcl-xl expression,protection of mitochondria,and blockage of mitochondria pathway of apoptosis.