TLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH.