Objective       To explore the role of 14-3-3γ gene in the protection of cardiomyocytes with lipopolysaccharide (LPS) pretreatment against anoxia/reoxygenation (A/R) injury.       Methods       A RNA interference (RNAi) recombinant plasmid of pSUPER/14-3-3γ was constructed and transferred into cardiomyocytes. The cardiomyocytes were divided into five groups including a control group

an A/R group

a LPS+A/R group

a pSUPER+LPS+A/R group and a pSUPER/14-3-3γ+LPS+A/R group. The protein level of 14-3-3γ was detected by Western blotting. The activity of lactate dehydrogenase (LDH) was determined by an automated biochemical analyzer. Cell viability was analyzed by MTT assay. Cell apoptosis was measured by flow cytometry. The opening of mitochondrial permeability transition pore (mPTP) was determined by swelling of isolated cardiac mitochondria.       Results       The A/R damage resulted in cell viability decrease

LDH and cell apoptosis increase

and mPTP opening. The LPS pretreatment up-regulated 14-3-3γ protein expression and protected cardiomyocytes against A/R injury through inhibiting the mPTP opening. The pSUPER/14-3-3γ RNAi recombinant plasmid could reduce 14-3-3γ protein expression and then reverse the protective effect of LPS pretreatment.       Conclusion       LPS pretreatment may have a protective effect on cardiomyocytes subjected to A/R injury

and its mechanism may be related to 14-3-3γ upregulation and subsequent mPTP opening inhibition.