Fever is common after intracerebral hemorrhage (ICH) though its molecular mechanism is unclear. In this study, we established a mouse model of ICH-fever and analyzed the molecular mechanism. The body temperature of adult male mice was measured with a telemeter implanted in the peritoneal cavity. To induce ICH, collagenase (Type VII) was injected into the brain under isoflurane anesthesia. When collagenase was injected into the preoptic area, the body temperature of mice started to elevate 30 min after the injection. It then reached the maximum level of 3ºC higher than the baseline between 4 h and 6 h after the injection. ICH was histologically confirmed 24 h after the injection. The elevation of body temperature was positively correlated with the ICH volume. Heat-inactivated collagenase neither induced ICH nor elevated the body temperature. When collagenase was injected into the striatum or pons, ICH was developed but the body temperature did not elevate. Intraperitoneal injection of diclofenac, a non-selective inhibitor of cyclooxygenase (COX), suppressed the elevation of body temperature after the collagenase injection into the preoptic area. On the other hand, NS398, a COX-2 selective inhibitor, did not suppress it. RT-PCR and immunohistochemistry revealed the presence of COX-1, COX-2 and mPGES-1 in the preoptic area after ICH. The present study established a mouse model of ICH-fever, in which COX-1-mediated elevation of prostaglandin (PG), possibly PGE2, seems to be essential. Although COX-2 is upregulated by ICH, its role in ICH-fever is unclear.