AIM To investigate the role of Nrf2/HO-1 in Kawasaki disease-induced myocardial injury in the rat model of Kawasaki disease by Lactobacillus casei cell wall extract (LCWE).
METHODS Sixty four-week old SD rats were randomly divided into control group, LCWE-induced Kawasaki disease group (LCWE) and TBHQ treatment group (KD+TBHQ). Control group was injected with 0.5 ml saline intraperitoneally, and KD group and KD+TBHQ group were injected with 0.5 ml LCWE (1 mg/ml) intraperitoneally. Four weeks later, rat cardiac functions were tested by ultrasonic testing, and myocardial malondialdehyde (MDA) content and activities of superoxide dismutase (SOD) and caspase-3 were detected by ELISA. Western blot was used to detect the protein level of nuclear factor-E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and apoptotic proteins Bcl-2 and Bax.
RESULTS Compared with those in control group, the left ventricular ejection fraction (EF) and fractional shortening (FS) were significantly decreased (P < 0.05) and the ratio of Bcl-2 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 protein level of Nrf2 and HO-1 were reduced (P < 0.05). TBHQ, the agonist of Nrf2, alleviated myocardial injury induced by KD and reduced the oxidative stress in myocardium (P < 0.05).
CONCLUSION KD can lead to oxidative stress, apoptosis and myocardial injury by inhibiting Nrf2/HO-1. TBHQ activates Nrf2/HO-1 which can inhibit myocardial apoptosis and improve cardiac functions.
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