The studies show the promising potential of bone marrow mononuclear cells (BMMC) for the treatment of stroke models. It is known that the BMMC are sensitive to environmental changes, like those induced by ischemia, such as events associated with inflammation. However, little is known about the biodistribution and survival of these cells in the post-injury nerve tissue. Aims to investigate whether the survival and spread of BMMC are influenced by the inflammatory response after striatum stroke. Heterologous transplantation (5x105 BMMC) in the striatum of rats clustered among untreated controls (CNT) and sham (SHM) and treated (STBC) perfused at 1, 3, 7 and 28 days. BMMC were impregnated with Qdot nanocrystals for identification by fluorescence microscopy in the host tissue. Staining for cresyl violet, and basic immunohistochemistry (IBA1 and ED1) were applied for histopathological analysis of tissue by light microscopy. Neurobehavioral tests (adhesive removal test and cylinder test) were performed to assess the response of groups for interventions. The results show the effectiveness of the experimental model of ischemic induction to reproduce the injury in the dorsolateral striatum. The cell infiltrate in the CNT group shows the inflammatory response, later confirmed by immunohistochemistry for ED1 and IBA1; the cellular infiltrate in STBM group, shows the BMMC of stay in all studied survival. The loss profile for death of BMMC transplanted into the injury site is similar between STBM and SHM groups, however, shows that inflammatory response of the receptor causes more decay of cell amount in STBM group. More refined or automated cell infusion procedures can improve the sensitivity of behavioral tests to discriminate the evolution between groups. To summarize the change of post-ischemic microenvironment creates conditions that determine the distribution and survival of BMMC. Other immunohistochemical procedures may point to the results presented as microglial profile and the degree of the immunomodulation study of the dynamics of inflammatory cytokines produced.
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