Abstract: Abstract Objective: To investigate the exogenous gene 14-3-3γ against cardiomyocyte damage induced by LPS, and explore the role of Bax of Bcl-2 family involving in the process. Methods: Neonatal SD rat cardiomyocytes were cultivated and constructed recombinant plasmid of pFLAG-14-3-3γ were transfected into the cells, which were treated with LPS subsequently. After treatment, 14-3-3γ levels were detected by western blotting, cells viability was analyzed by MTT, the activity of LDH and CPK were determined by auto-biochemistry analysator, the levels of Bax protein in cytoplasm and mitochondria were detected by western blotting. Results: 14-3-3γ protein significantly increased in the cardiomyocytes transfected by pFLAG-14-3-3γ. Compared with control group, cardiomyocytes treated with LPS had significantly reduced cells viability(P<0.01), increased LDH and CPK activities(P<0.01), and promoted Bax translocation from cytoplasm to mitochondria. Elevated l4-3-3γ protein resulted by transfection of pFLAG-14-3-3γ reversed cardiomyocytes damage induced by LPS. Compared with untransfected group, cardiomyocytes of transfected group had significantly increased cells viability(P<0.01), decreased LDH and CPK activities(P<0.01), and inhibited Bax translocation from cytoplasm to mitochondria. Conclusion: 14-3-3γ protects cardiomyocytes against LPS damage by inhibiting Bax translocation from cytoplasm to mitochondria.

Key words: LPS, myocardial damage, gene recombination, 14-3-3γ, transfection, Bax