AIM  To investigate the role of resveratrol (Res) in Kawasaki disease-induced myocardial injury and whether the mechanism was related to Sirt1/Nrf2 signaling pathway.

  METHODS  Sixty four-weeks old SD rats were randomly divided into control group, LCWE-induced Kawasaki disease group (KD), Res treatment group (Res + KD) or Res and EX527 co-treatment group (Res + EX527 + KD). Control group was injected with 0.5 ml saline intraperitoneally, while KD group, Res + KD group and Res + EX527 + KD group were injected with 0.5 ml LCWE (1 mg/ml) intraperitoneally. Four weeks later, the rat cardiac functions were detected by ultrasonic testing, and myocardial malondialdehyde (MDA) content, superoxide dismutase (SOD) and caspase-3 activity were detected by ELISA. The protein levels of Sirt1, nuclear factor-E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and apoptotic proteins Bcl2 and Bax were detected by Western blot.

  RESULTS  Compared with those in control group, the left ventricular ejection fraction (LVEF) and fractional shortening (FS) were significantly decreased in KD group (P < 0.05) and the ratio of Bcl2 and Bax was also decreased (P < 0.05). The caspase-3 activity and myocardial MDA content were increased (P < 0.05), while SOD activity and the protein levels of Sirt1, Nrf2 and HO-1 were reduced (P < 0.05). Res could alleviate myocardial injury induced by KD and reduce the oxidative stress in myocardium (P < 0.05). These effects were blocked by EX527.

  CONCLUSION  KD can lead to oxidative stress, apoptosis and myocardial injury by inhibiting Sirt1/Nrf2 signaling. Res activates Sirt1/Nrf2, which can inhibit myocardial apoptosis and improve cardiac functions in KD-induced myocardial injury.