The objectives were to evaluate alterations in ischemic rat pups, from dams administered with curcumin (25 and 50？mg/kg). Ten-day-old male pups were subjected or not (SO) to brain ischemia and reperfusion, for 1, 7, and 14 days (this last group was submitted to behavioral evaluation). After that, pups were euthanized for determinations of striatal DA and DOPAC in SO, ischemic from untreated (ICUD) or curcumin treated (ICTD) dams, as well as hippocampal immunohistochemistry assays for iNOS and COX-2 and cresyl violet staining. At the 14th postischemia day, the ICUD group showed increased locomotor activity and rearing behavior, which were reversed in ICTD animals. ICUD pups presented decreased striatal DA and DOPAC levels, relatively to SO, mainly at the 1st postischemia day, but also at the 7th and 14th days which were partially reversed in ICTD pups. A greater number of viable neurons were observed in ICTD, as related to the ICUD group. Ischemia increased iNOS and COX-2 expressions, in CA1 and CA3 areas, at the 1st, 7th, and 14th postischemia days, and these effects were minimized in ICTD pups. In conclusion, the prenatal curcumin treatment was shown to be neuroprotective where the drug anti-inflammatory and antioxidant effects probably play a role. 1. Introduction Cerebral ischemia is a very common cerebrovascular disease and one leading cause of morbidity and mortality worldwide, whose complex pathology includes inflammatory events, as aggregation of inflammatory cells and upregulation of cytokines [1]. Furthermore, hypoxic-ischemic brain damage is a major cause of acute mortality and chronic neurologic morbidity, in infants and children. Much of our understanding on mechanisms of hypoxic-ischemic brain damage and potential therapeutic interventions derive from experimental models in the adult animal. It is accepted that a cerebral hypoxic-ischemic event of sufficient severity to deplete tissue energy reserves is rapidly followed by acidosis, glutamate excitotoxicity, generation of reactive oxygen species, and oxidative stress, followed by prolonged periods of delayed cell death and inflammation [2]. However, direct application of adult brain findings to the newborn animal is not a simple task, since the immature brain is generally considered resistant to the damaging effects of hypoxia and ischemia. At the same time, the immature brain exhibits periods of heightened sensitivity to injury, dependent upon the brain specific developmental stage [2]. Cerebral ischemia causes disturbances in a variety of cellular and molecular mechanisms, including
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