Intra-cerebral hemorrhage (ICH) represents 10–15% of all strokes, and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke [1]. The mortality of ICH is higher than that of ischemic stroke. Only 31% are functionally independent at 3 months. Only 38% of the patients survive the 1st year [10]. Unfortunately, the method for treatment of this disease and protection of the brain tissue after ICH are not effective. Mass effect, ischemia, and toxicity of blood components after ICH induce brain tissue damage. In addition, there is increasing evidence that inflammatory processes are involved in cerebrovascular events. After ICH, inflammatory mediators from the blood might enter to the brain and induce an inflammatory reaction and the brain cells itself are also capable of producing many of these agents [11]. The inflammatory responses are responsible for the ICH induced brain injury, which could provide new therapeutic targets for ICH. Various constituents of the inflammatory response, including adhesion molecules, cytokines, leukocytes, immunoglobulins, and complement, may be important in the pathogenesis of ICH. However, how the inflammatory responses is activated and regulated in the brain tissue after ICH is unclear.