To investigate the impact of quercetin (Que) on myocardial ischemia-reperfusion injury in rats and to elucidate its underlying mechanisms.

A rat model of myocardial ischemia-reperfusion was created by occluding the left anterior descending artery. A total of 60 SD rats were randomly divided into sham group, model group, low-dose experimental group (20 mg·kg^-1 Que), high-dose experimental group (80 mg·kg^-1 Que) and inhibitor group (80 mg·kg^-1 Que+3 mg·kg^-1 MCC950), with 12 rats in each group. Echocardiography was conducted after 14 days of continuous administration to assess the relevant indicators of cardiac function. Rat serum was taken and the amounts of serum myocardial damage indicators and inflammatory factors were detected by kit method. Western blotting was used to determine the relative expression levels of Toll-like receptor 2 (TLR2)/ nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) - related proteins in the rat myocardial tissue.

The left ventricular ejection fraction of rats in sham group, model group, low-dose experimental group, high-dose experimental group and inhibitor group were (79.36±5.37)%, (42.85±3.96)%, (48.51±4.20)%, (71.66±5.14)% and (55.73±4.68)%, respectively; the troponin Ⅰ (cTnⅠ) levels were (0.07±0.01), (0.38±0.03), (0.25±0.03), (0.13±0.01) and (0.20±0.02) ng·mL^-1, respectively; the interleukin-1β (IL-1β) levels were (1.01±0.15), (3.43±0.22), (2.65±0.26), (1.39±0.23) and (1.61±0.13) ng·mL^-1, respectively; the relative expression levels of TLR2 protein were 0.33±0.05, 1.01±0.07, 0.73±0.05, 0.45±0.03 and 0.50±0.06, respectively; the relative expression levels of NLRP3 protein were 0.34±0.06, 1.05±0.09, 0.86±0.07, 0.39±0.06 and 0.56±0.05, respectively. Compared with sham group, the model group showed statistically significant differences in the above indicators (all P<0.05); compared with model group and high-dose experimental group, the low-dose experimental group also exhibited statistically significant differences in the above indicators (all P<0.05).

Quercetin can alleviate myocardial ischemia-reperfusion (I/R) injury in rats and improve cardiac function. The mechanism may be related to the inhibition of the TLR2/NLRP3 inflammatory signaling pathway. Quercetin may exert its cardioprotective effect by down-regulating the expression of TLR2, thereby blocking its activation of the downstream NLRP3 inflammasome, containing NLRP3 and apoptosis-associated speck-like protein containing a CARD (ASC) and ultimately reducing the release of pro-inflammatory factors such as IL-1β.