“…These inflammatory cytokines could cause disturbed energy metabolism (Schilling et al, ), impaired β‐adrenergic signaling(de Montmollin, Aboab, Mansart, & Annane, ), imbalanced calcium homeostasis (Zhong, Hwang, Adams, & Rubin, ), and excess production of nitric oxide (Stein, Frank, Schmitz, Scholz, & Thoenes, ), all of which resulted in impaired contractility, diastolic dysfunction, reduced cardiac index, and ejection fraction (de Montmollin et al, ; Schilling et al, ; Stein et al, ; Zhong et al, ). In previous studies, myricetin has been showed to protect the mouse or rat heart from isoproterenol induced myocardial infarction(Tiwari, Mohan, Kasture, Maxia, & Ballero, ), ischemia/reperfusion induced injury (Scarabelli et al, ), and hypertension (Borde, Mohan, & Kasture, ), and the underlying mechanism was related to the regulation of Stat1 and oxidative stress (Borde et al, ; Scarabelli et al, ; Tiwari et al, ). In in vitro experiments, myricetin could blunt the activation of NF‐κB and inhibit the production of proinflammatory cytokines in H9C2 cardiomyocytes (Chen & Fan, ) and macrophages (Cho et al, ).…”