["Ticagrelor inhibits the equilibrative-nucleoside-transporter-1 and thereby, adenosine cell re-uptake. Ticagrelor limits infarct size (IS) in non-diabetic rats and the effect is adenosine-dependent. Statins, via ecto-5'-nucleotidase activation, also increase adenosine levels and limit IS.", 'Ticagrelor and rosuvastatin have additive effects on myocardial adenosine levels, and therefore, on IS and post-reperfusion activation of the NLRP3-inflammasome.', 'Diabetic ZDF rats received via oral gavage; water (control), ticagrelor (150\xa0mg/kg/d), prasugrel (7.5\xa0mg/kg/d), rosuvastatin (5\xa0mg/kg/d), ticagrelor\xa0+\xa0rosuvastatin and prasugrel\xa0+\xa0rosuvastatin for 3d. On day 4, rats underwent 30\xa0min coronary artery occlusion and 24\xa0h of reperfusion. Two additional groups received, ticagrelor\xa0+\xa0rosuvastatin or water in combination with CGS15943 (CGS, an adenosine receptor antagonist, 10\xa0mg/kg\xa0i.p. 1\xa0h before ischemia).', 'Both ticagrelor and rosuvastatin increased myocardial adenosine levels with an additive effect of the combination whereas prasugrel had no effect. Similarly, both ticagrelor and rosuvastatin significantly reduced IS with an additive effect of the combination whereas prasugrel had no effect. The effect on IS was adenosine dependent as CGS15943 reversed the effect of ticagrelor\xa0+\xa0rosuvastatin. The ischemia-reperfusion injury increased myocardial mRNA levels of NLRP3, ASC, IL-1β and IL-6. Ticagrelor and rosuvastatin, but not prasugrel, significantly decreased these pro-inflammatory mediators with a trend to an additive effect of the combination. The combination also increased the levels of anti-inflammatory 15-epilipoxin A'] Do ticagrelor and Rosuvastatin Have Additive Cardioprotective Effects via Adenosine?