Inflammatory response in the nervous system, called neuroinflammation, is a common process of several neurodegenerative diseases and brain disorders. To understand the underlying mechanism of this brain response to damage would be interesting to identify new common therapy targets to neurodegenerative processes. Ischemic stroke has an important socioeconomic impact being the second cause of mortality and the first cause of long-term disability in the world. Until now, there is not any pharmacological treatment to reduce the brain damage induced. In this review, we will expose recent evidences about neuroinflammation after stroke in animal models and in human. We summarize the most relevant information about the inflammatory-cellular component: microglia/ astrocytes response and peripheral blood cells infiltration to the brain describing the key adhesion molecules implicated in this process. Also, we review the inflammatory-molecular response including the beneficial/detrimental role of chemokines and cytokines after ischemia. Currently, female sexual hormones (estradiol and progesterone) are considered as neuroprotective agents. We and others laboratories demonstrated anti-inflammatory actions of these hormones after stroke, modulating not only the cellular response (reducing the reactive gliosis), but also the immune response. Here, we will present the current data about the neuroprotective role of estradiol and progesterone after ischemic injury focused in their anti-inflammatory action. Additionally, we will review the recent information about the mechanism of action of both hormones, including different receptors and signaling pathways. Finally, we will discuss the synergistic or antagonic therapeutic effects when they are administered together.