Ischemic stroke is a devastating clinical event. Increasing evidence suggests that inflammatory mechanisms are involved in the progression of post ischemic-induced brain injury. Cerebral ischemia is accompanied by a marked inflammatory reaction that is initiated by ischemia-induced expression of cytokines, adhesion molecules, and other inflammatory mediators, including prostanoids, extracellular proteases, reactive oxygen species and nitric oxide, leading to the accumulation of inflammatory cells, such as leukocytes and microglia. The inflammatory reaction, which has a rapid onset and continues after the stroke, is thought to acutely contribute to the evolution of tissue injury. Many compounds have been identified in cerebral ischemia, which are known to promote and sustain inflammatory responses. Better understanding of the role of the post ischemic-induced inflammatory response and its potential for modulation might have profound implications for patient treatment. Pre-clinical studies suggest that interventions that are aimed at attenuating such inflammation reduce the progression of brain damage that occurs during the late stages of cerebral ischemia. In particular, strategies that block the activity of inflammation-related enzymes reduce ischemic damage with an extended therapeutic window. In this review, a summary of the available literature on the inflammatory responses after cerebral ischemia and ischemic stroke is presented along with discussion of some of the emerging opportunities for potential therapeutic strategies. Although at the moment, clinical trials using anti-inflammatory strategies did not show benefit in patients with ischemic stroke, there is a strong rationale for continuing to explore the efficacy of anti-inflammatory therapies in the treatment of the late stages of cerebral ischemia. It is plausible that in the near future, additional strategies using neuroprotective drug cocktails that target inflammation could offer exciting new promise in the therapeutic approach to ischemic stroke.