Abstract: Objective　To investigate the role of silent mating type information regulator 2 homolog 3 (SIRT3) -forkhead box O1(FOXO1) pathway-mediated autophagy in myocardial ischemia-reperfusion (IR) injury. Methods　SIRT3 overexpression stable strain was constructed by lentivirus infection of H9C2 cells. The cells were divided into four groups: the normal control (NC) group, the ischemia-reperfusion (IR) group, the SIRT3 overexpression +IR (S+IR) group and the SIRT3 overexpression +IR+ SIRT3 inhibitor (S+IR+3-TYP) group. The expressions of SIRT3, Ac-FOXO1, autophagy labeled protein LC3B, Beclin1 and apoptotic proteins Bcl-2 and Bax were detected by Western blot assay. The apoptosis rate was detected by flow cytometry. The level of lactate dehydrogenase (LDH) in the supernatant of cell culture was determined by automatic biochemical analyzer. Results　Compared with the NC group, the expression of SIRT3 was decreased, Ac-FOXO1 was increased, the expressions of autophagy related proteins Beclin1 and LC3B were increased, the expression of anti-apoptotic protein Bcl-2 was decreased, the expression of pro-apoptotic protein Bax was increased, LDH release and cell apoptosis rate were increased in the IR group (P＜0.05). Compared with the IR group, the expression of SIRT3 increased, Beclin1, LC3B and Bcl-2 were increased, the expressions of Ac-FOXO1, pro-apoptotic protein Bax were decreased, LDH release and cell apoptosis rate were decreased in the S+IR group (P＜0.05). After adding SIRT3 inhibitor 3-TYP, there was no significant change in SIRT3 expression compared with that of the S+IR group, but the expression of Ac-FOXO1 was increased, the expressions of Beclin1 and LC3B were decreased, the expression of anti-apoptotic protein Bcl-2 was decreased, the expression of pro-apoptotic protein Bax was increased, LDH release and cell apoptosis rate were increased (P＜0.05). Conclusion　The activation of SIRT3-FOXO1 pathway can increase autophagy level of H9C2 cells, and has a protective effect on myocardial ischemia reperfusion injury.

Key words: myocytes, cardiac, reperfusion injury, autophagy, apoptosis, forkhead box protein O1, silent mating type information regulator 2 homolog 3, H9C2 cell