Objective      To determine the effects of a transcription factor

Yin Yang 1 (YY1) on the apoptosis of cardiomyocytes induced by ischemic hypoxia and investigate the related mechanisms.       Methods      Cardiomyocytes were isolated from neonatal rat heart tissue and then cultured in vitro. Sugar-free culture medium and Billups-rothenberg (95%N

2

+5%CO

2

) was used to induce the apoptosis of cardiomyocytes. Plasmid of YY1 overexpression was established and then tansfected into the cardiomyocytes. Then the cells were divided into 6 groups of cells

that is

normal control group

YY1 group

ischemic hypoxia group

ischemic hypoxia+YY1 group

ischemic hypoxia+LY294002 group and ischemic hypoxia+YY1+LY294002 group. The viability of cardiomyocytes of above groups was measured by CCK-8 assay. Cell apoptosis was measured with TUNEL assay. The mRNA expression of YY1 was detected by real-time quantitative PCR. The expression levels of YY1

phosphorylated Aktser473 and survivin were detected by Western blotting.       Results      Compared with the normal control group

the viability was significantly decreased (0.55±0.02 vs 1.14±0.02

P0.01) and the apoptosis increased [(38.25±1.65)% vs (1.38±0.15)%

P0.01

]

in the ischemic hypoxia treatment group after 6 hours′ ischemia-hypoxia stimulation. But transfection of YY1 overexpression plasmid prior to ischemic hypoxia stimulation could significantly reverse the phenomena [0.78±0.03 vs 0.55±0.02

(14.50±1.56)% vs (38.25±1.65)%

P0.01

]

and enhanced the protein levels of p-Aktser473 and survivin (0.82±0.03 vs 0.28±0.03

0.93±0.02 vs 0.36±0.02

P0.01). However

the inhibitor of PI3K/Akt signal pathway

LY294002

suppressed the cell viability (0.62±0.02 vs 0.78±0.03

P0.01) and apoptosis [(27.75±1.12)% vs (14.50±1.56)%

P0.01

]

and repressed the expression levels of p-Aktser473 (0.43±0.02 vs 0.82±0.03

P0.01) and survivin (0.27±0.02 vs 0.93±0.02

P0.01) induced by YY1 plasmid transfection

.       Conclusion      YY1 inhibits the apoptosis in ischemic hypoxia-induced cardomyocytes

which may be mediated by activation of PI3K/Akt signal pathway.