Ticagrelor attenuates myocardial ischaemia–reperfusion injury possibly through downregulating galectin‐3 expression in the infarct area of rats

AIMS: The full benefits of myocardial revascularization strategies applied to acute myocardial infarction patients might be reduced by myocardial ischaemia and reperfusion (I/R) injury. It is known that inflammation plays an important role in the pathogenesis of I/R injury and galectin‐3, a known inflammatory factor, is actively involved in ischaemia‐induced inflammation and fibrosis of various organs. Previous studies demonstrated that anti‐platelets therapy with ticagrelor, a new P2Y12 receptor antagonist, could effectively attenuate myocardial I/R injury and I/R injury‐related inflammatory responses. It remains unknown whether the cardioprotective effects of ticagrelor are also mediated by modulating myocardial galectin‐3 expression. METHODS: We determined the ratio of infarct area (IA)/area at risk (AAR), expression of galectin‐3, TNF‐α and IL‐6 in infarct area of rats treated with placebo (equal volume saline per gastric gavage immediately after LAD ligation, then once daily till study end) or ticagrelor (150 mg kg(−1) dissolved in saline per gastric gavage immediately after LAD ligation, then once daily till study end) at 24 h, 3 and 7 days post I (45 min)/R injury. Sham‐operated rats served as control. RESULTS: Our results showed that ticagrelor treatment significantly reduced IA/AAR ratio at 3 and 7 days post I/R, downregulated mRNA and protein expression of galectin‐3, as well as mRNA expression of TNF‐α and IL‐6 in infarct area at 24 h, 3 and 7 days post I/R. CONCLUSIONS: Our results suggest that the cardioprotective effects of ticagrelor might partly be mediated by downregulating galectin‐3 expression in infarct area in this rat model of myocardial I/R injury.