Background: DIC is one of the most used nonsteroidal anti-inflammatory drugs (NSAIDs) and despite its extensive therapeutic utility, diclofenac may cause multiple severe side effects, including renal injury and hepatotoxicity. Ticagrelor beside its potent antiplatelet activity has anti-inflammatory, anti-oxidative and anti-apoptotic effect, herein, we will study its possible protective effect against DIC induced hepatorenal toxicity. Aim: To assess the possible protective effects of ticagrelor against hepatic toxicity and renal toxicity induced by diclofenac Methods: Fifty four male albino rats, weighing 200-250 g, were used randomly allocated to nine groups each one contain 6 rats as follow: Group 1(Control negative): given saline orally for 28 days. Group 2 (Ticagrelor): given ticagrelor alone (20 mg/kg/day, orally) for 7 days. Group 3 (Diclofenac): given diclofenac (10 mg/kg/day, i.p.) for 7 days. Group 4 (s Small dose prophylactic group (SP)): given ticagrelor (10 mg/kg/day, orally) concomitantly with diclofenac (10 mg/kg/day, i.p.) for 7 days. Group 5 (Large dose prophylactic group (LP)): given ticagrelor (20 mg/kg/day, orally) concomitantly with diclofenac (10 mg/kg/day, i.p.) for 7 days. Group 6 (Short term small dose treatment group (SST)): given diclofenac as in Group 3, followed by ticagrelor (10 mg/kg/day, orally) for another 7 days. Group 7 (Short term large dose treatment group (SLT)): v diclofenac as in Group 3, followed by ticagrelor (20 mg/kg/day, orally) for another 7 days. Group 8 (Long term small dose treatment group (LST)): given diclofenac as in Group 3, followed by ticagrelor (10 mg/kg/day, orally) for another 28 days. Group 9 (Long term large dose treatment group (LLT)): given diclofenac as in Group 3, followed by ticagrelor (20 mg/kg/day, orally) for another 28 days. At the end of the experiment, the following parameters were measured: Portal blood pressure (cm/H2O), liver and kidney functions, Serum ASC, mTOR, NLRP3, IL1, Serum GSDMD, caspase1, superoxide dismutase levels(SOD), Hepatic and renal MDA and histopathological examination. Results: The results of this work showed that diclofenac (10 mg/kg/day, i.p.) for 7 days produced hepatotoxicity and nephrotoxicity by decreasing serum SOD level and by increasing serum AST, ALT, hepatic MDA, portal blood pressure ,serum urea , creatinine ,renal MDA ,serum NLRP3 ,ASC, mTOR ,GSDMD ,IL1 ,caspase1 levels and microscopic scoring of renal and hepatic tissues. While ticagrelor (10 and 20mg/kg/day, orally) produced a prophylactic effect by increasing serum SOD level and by decreasing serum AST, ALT, hepatic MDA ,portal blood pressure ,serum urea, creatinine ,renal MDA ,serum NLRP3 ,ASC, mTOR ,GSDMD ,IL1 ,caspase1 levels and microscopic scoring of renal and hepatic tissues in a dose dependent manner. The results of this work also showed that ticagrelor (10 and 20mg/kg/day, orally) for 7 and 28 days produced a curative effect by increasing serum SOD level and by decreasing serum AST, ALT, hepatic MDA ,portal blood pressure ,serum urea , creatinine ,renal MDA ,serum NLRP3 ,ASC, mTOR ,GSDMD ,IL1 ,caspase1 levels and microscopic scoring of renal and hepatic tissues .The effect of ticagrelor ( 20mg/kg/day, orally) for 28 days produced the most significant results. Conclusion: In light of the results of this study we concluded that ticagrelor in a dose of 10 and 20 mg/kg was proved to have prophylactic and curative effect against diclofenac induced hepatotoxicity and nephrotoxicity by its antioxidant, anti-inflammatory and anti-apoptotic effect but further experimental studies are required to confirm our results