AIM  To investigate the protective effect of triiodothyronine (T₃) on mice cardiomyocytes under ischemia/reperfusion (I/R) injury.

  METHODS  Thirty Kunming mice were randomly divided into 5 groups, including a sham operation group,an I/R group, an I/R + T₃ group,an I/R + T₃ + PI3K/Akt signaling blocker (I/R + T₃ + LY294002) group and an I/R + PI3K/Akt signaling blocker (I/R + LY294002) group. T₃ 2 μg/100（mg.d） and LY294002 30 μg/100（mg.d） were administered intraperitoneally once a day for 3 consecutive days before I/R. One week later, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione (GSH) and mitochondrial superoxide levels were detected in each group. The pathological changes of myocardial tissues were observed and the mice cardiac functions in each group were detected by echocardiography.

  RESULTS  Compared with those in the sham group, SOD, GSH-Px and GSH levels in the I/R group decreased significantly (P < 0.05) while the superoxide levels in myocardial mitochondria were significantly increased (P < 0.01). Pathological changes such as infiltration of inflammatory cells, breakage of muscle fibers, and disorder of arrangement were found in the I/R-induced myocardial tissue. In the I/R-induced mice, the left ventricular ejection fraction (LVEF) and fractional shortening rate (FS) were decreased markedly, and the left ventricular end systolic diameter (LVDs), left ventricular end diastolic diameter (LVDd), and the heart to body weight rate were significantly increased (P < 0.01). Compared with those in the I/R group, SOD, GSH- Px and GSH levels in the I/R + T₃ group were significantly increased (P < 0.01), while the levels of superoxide in myocardial mitochondria were decreased (P < 0.01). Pathological changes such as infiltration of inflammatory cells, breakage of muscle fibers, and disorder of arrangement were alleviated in the I/R + T₃ group. The LVEF and FS were significantly increased, and LVDs and the heart to body weight were decreased in the I/R + T₃ group (P < 0.05). Compared with those in the I/R + T₃ group, the levels of SOD, GSH-Px, and GSH in the I/R + T₃ + LY294002 group decreased significantly (P <0.05) and the myocardial mitochondrial superoxide levels increased (P < 0.01). Pathological changes such as infiltration of inflammatory cells, breakage of muscle fibers, and disorder of arrangement were aggravated in the I/R+T₃ + LY294002 group. The values of LVEF and FS in mice were decreased and the LVDs and heart/body weight in mice were significantly increased in the I/R + T₃ + LY294002 group (P < 0.05).

  CONCLUSION  Thyroid hormone can protect myocardium against I/R injury through antioxidant damage, which may be partly achieved by activating the PI3K/Akt signaling pathway.