Toll-like receptors (TLRs) are a family of signal transduction molecules and play a critical role in the induction of innate and adaptive immunity [4]. TLR-mediated signaling pathways mainly stimulate the activation of NFκB [12, 13]. TLR4, the first mammalian TLR recognized, has been reported to be involved in several central nervous (CNS) system diseases, such as inflammatory or autoimmune CNS diseases and cerebral ischemic injury [7, 8]. Although previous reports indicated that the activation of NFκB was attributed to the oxidative stress or glutamate receptor activation induced by red blood cells and/or plasma constituents [17], very few studies have been directed to investigate the role and the relationship between TLR4-mediated NFκB signaling and ICH.