Resveratrol alleviates Kawasaki disease-induced myocardial injury via inhibition of apoptosis and autophagy.

Objectives: To explore the effect of resveratrol (Res) on Kawasaki disease (KD)-induced myocardial injury and to evaluate its effect on apoptosis and autophagy.
Methods: Forty-eight juvenile male Sprague Dawley rats were randomly divided into a control group, a Res group, a lactobacillus casei cell wall extract (LCWE)-induced Kawasaki disease group (KD group), and a LCWE-induced Kawasaki disease + Res treatment group (Res+KD group). The control group was intraperitoneally injected with saline. The Res group was intraperitoneally injected with resveratrol (100 mg/kg). The KD group was intraperitoneally injected with 0.5 mL LCWE (1 mg/mL). The Res+KD group was intraperitoneally injected with 0.5 mL LCWE (1 mg/mL) and resveratrol (100 mg/kg). After 4 weeks, the left ventricular ejection fraction (LVEF) and short axis shortening rate (LVFS) were detected by echocardiography. The apoptotic rate was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) staining. The levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), microtubule-associated protein 1 light chain 3β (LC3B), Beclin-1, autophagy related 5 (Atg5) and sequestosome-1 (p62) were detected by Western blotting. The formation of autophagosome was observed under transmission electron microscope.
Results: There was no significant difference in the above-mentioned indexes between the control group and the Res group (all P >0.05). Compared with the control group, the values of LVEF and LVFS were significantly decreased in the KD group (both P <0.01); the ratio of Bax/Bcl-2 and TUNEL-positive cells were increased (both P <0.01); the LC3BII/LC3BI ratio, the levels of Beclin 1, Atg5 and p62, and the number of autophagosomes were also significantly increased in KD group (all P <0.01). Compared with the KD group, the values of LVEF and LVFS were significantly increased, the ratio of Bax/Bcl-2 and TUNEL-positive cells were decreased, the LC3BII/LC3BI ratio, the levels of Beclin 1, Atg5 and p62 were all decreased (all P <0.01), and the number of autophagosomes was suppressed.
Conclusions: Res can attenuate the KD-induced myocardial injury via inhibiting the apoptosis and autophagy.