The administration of butyrate resulted in a decrease in brain damage, inhibition of the synthesis of inflammatory markers such as IL-1β and chemokine CXCL10, and prevented the overexpression of COX-2 in the injured hemisphere affected by ischemia. In addition, the administration of butyrate facilitated the transition of microglia phenotypic from an inflammatory M1 state to an anti-inflammatory M2 state. The gene discussed is CXCL10; the disease is ischemia.