Abstract: Objective: To study the effection of Helix B surface peptide(HBSP) to myocardial apoptosis in the state of acute anoxia / reoxygenation and its possible mechanism. METHODS: CμLtured neonatal rat cardiomyocytes H9C2 cell line in vitro and establishment anoxia (3h) / reoxygenation (3h) model. The experiment were divided into three group: control group, anoxia / reoxygenation group (A/R) and H / R + HBSP groups. CμLture supernatants were collected to measure the lactate dehydrogenase (LDH) levels and the myocardial apoptosis rate was detected by using Annexin-V and PI double staining and flow cytometry. What’s more, Western blot analysis was used to measure the expression of cytochrome C, and the activities of caspase-3 and caspase-9 were determined by a colorimetric method. ResμLts: Compared with the control group, cell viability and mitochondrial cytochrome C protein levels in A/R group were significantly decreased（P<0.01）, while the rate of apoptosis, caspase-9, caspase-3 activity and cytosolic cytochrome C protein levels were significantly increased（P <0.01）. Conclusion: HBSP significantly protect neonatal rat cardiomyocytes from the injury of anoxia /reoxygenation and the mechanism may be inhibiting the cell apoptotic mediated by mitochondrial pathway.

Key words: HBSP, anoxia / reoxygenation, myocardial cells, apoptosis, mitochondrial pathway