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Paraquat (PQ) is an herbicide toxin that induces injury in different organs. The anti‐inflammatory and antioxidant effects of carvacrol were reported previously. The effects of carvacrol and pioglitazone (Pio) alone and their combination on inhaled PQ‐induced systemic and lung oxidative stress and inflammation as well as behavioral changes were examined in rats. In this study, animals were exposed to saline (control [Ctrl]) or PQ (PQ groups) aerosols. PQ‐exposed animals were treated with 0.03 mg/kg/day dexamethasone (Dexa), 20 and 80 mg/kg/day carvacrol (C‐L and C‐H), 5 mg/kg/day Pio, and Pio+C‐L for 16 days. Inhaled PQ markedly enhanced total and differential white blood cell (WBC) counts, nitric oxide (NO), and malondialdehyde (MDA) levels but decreased catalase (CAT) and superoxide dismutase (SOD) activities and thiol levels both in the bronchoalveolar lavage fluid (BALF) and blood and increased interferon‐gamma (INF‐γ) and interleukin‐10 (IL‐10) levels in the BALF (p < 0.001 for all cases) except lymphocyte count in blood which was not significantly changed. The escape latency and traveled distance were increased in the PQ group. However, the time spent in the target quadrant in the Morris water maze (MWM) test and the duration of time latency in the dark room in the shuttle box test were reduced after receiving an electrical shock (p < 0.05–p < 0.001). Inhaled PQ‐induced changes were significantly improved in carvacrol, Pio, Dexa, and especially in the combination of the Pio+C‐L treated groups (p < 0.05–p < 0.001). Carvacrol and Pio improved PQ‐induced changes similar to Dexa, but ameliorative effects produced by combination treatments of Pio+C‐L were more prominent than Pio and C‐L alone, suggesting a potentiating effect for the combination of the two agents. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) is a well‐known pathological condition that is characterized by high morbidity and mortality. The main pathological manifestation of CAD is myocardial injury due to ischemia–reperfusion (I–R). Currently, no efficacious treatment of protecting the heart against myocardial I–R exists. Hence, it is necessary to discover or develop novel strategies to prevent myocardial‐reperfusion injury to improve clinical outcomes in patients with CAD. A large body of experimental evidence supports cardioprotective properties of curcumin and the ability of this phytochemical to modify some cardiovascular risk factors. However, the detailed effects of curcumin in myocardial I–R injury are still unclear and there is a lack of evidence concerning which curcumin regimen may be ideal for myocardial I–R injury. This paper presents a brief review of the pathophysiology of myocardial I–R injury and the mechanisms of action of curcumin in reducing myocardial I–R injury. Coronary artery disease (CAD) is a well‐known pathological condition that is characterized by high morbidity and mortality; the main pathological manifestation of CAD is myocardial injury due to ischemia–reperfusion (I–R). Currently, no efficacious treatment for protecting the heart against myocardial I–R exists; hence, it is necessary to discover or develop novel strategies to prevent myocardial‐reperfusion injury to improve clinical outcomes in patients with CAD. A large body of experimental evidence supports cardioprotective properties of curcumin and the ability of this phytochemical to modify some cardiovascular risk factors, but the detailed effects of curcumin in myocardial I–R injury are still unclear and there is a lack of evidence concerning which curcumin regimen may be ideal for myocardial I–R injury. Therefore, this paper presents a brief review of the pathophysiology of myocardial I–R injury and the mechanisms of action of curcumin in reducing myocardial I–R injury. [ABSTRACT FROM AUTHOR]