As we reported previously (Acta Neurochir Suppl., 2003), disruption of cytosolic phospholipase A2 (cPLA2) resulted in significant reduction of infarct area and neurological deficit severity in the MCA occlusion model using cPLA2 deficient mice. But the exact mechanism of protection and main target of cPLA2 disruption in CNS have been still unknown. After a cerebral infarction, there is an acute inflammatory response with entry of neutrophils, macropharges, and other blood elements into the ischemic zone. The current study was to investigate the contribution of bone marrow-derived cells in the mechanism. We transplanted bone marrow from male cPLA2 deficient mice into female C57BL/6J mice. Achievement of transplantation was confirmed by existence of Y chromosome. Approximately 4 month after transplantation, the recipient mice underwent suture occlusion of middle cerebral artery (MCA) and reperfusion. Quantification of cerebral infarction was determined by TTC staining followed by volumetric analysis of digitized image. Neurological deficit was evaluated according to modified 4-point scale as described previously. The infarction volume of recipient mice transplanted with cPLA2 deficient mice tend to be smaller than the mice transplanted with wild type mice but not statistically significant. The neurological deficit score also revealed no significant difference. There are some underlying problems for the evaluation of results. We report the preliminary results and discuss those problems.
