Treatment with bone marrow mononuclear cells induces  functional recovery and decreases neurodegeneration after  sensorimotor cortical ischemia in rats.
We evaluated the beneficial effect of treatment with bone marrow mononuclear cells(BMMC) in a rat model of focal ischemia induced by thermocoagulation of the blood vessels in the left sensorimotor cortex. BMMC were obtained from donor rats and injected into the femoral vein one day after ischemia. BMMC-treated animals received approx. 3×10⁷ cells and control animals received PBS. Animals were evaluated for functional sensorimotor recovery weekly with behavioral tests and for changes in neurodegeneration and structural plasticity with histochemical and immunostaining techniques, respectively. The BMMC-treated group showed a significant recovery of function in the cylinder test 14, 21 and 28 days after ischemia. In the beam test, both groups showed improvement, with a tendency for faster recovery in the BMMC-treated group. In the adhesive test, both groups did not show significant recovery of function. FJC+ cell counting revealed significant decrease in the neurodegeneration in the periphery of the lesion in the BMMC-treated group. The analyses by immunoblotting revealed no significant difference in the expression of GAP-43 and synaptophysin between the groups. Thus, our results showed beneficial effects of the treatment with BMMC, which promoted significant functional recovery and decreased neurodegeneration. These results suggest that the therapy with BMMC is effective and might be a protocol of treatment for stroke in humans, alternative to the therapy proposed with the bone marrow-derived mesenchymal stem cells.
Laboratório de Neurobiologia Celular e Molecular, Instituto de Biofísica Carlos Chagas Filho, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho, 373, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ, CEP: 21941-902, Brazil.
Arthur
A
Giraldi-Guimardes
Maíra
M
Rezende-Lima
Fernando Pereira
FP
Bruno
Rosalia
R
Mendez-Otero
D000818:Animals; D001369:Axons / Q000378:metabolism / Q000473:pathology; D016026:Bone Marrow Transplantation; D002545:Brain Ischemia / Q000378:metabolism / Q000628:therapy*; D019922:GAP-43 Protein / Q000378:metabolism; D008297:Male; D009043:Motor Activity; D009474:Neurons / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function; D066191:Sensorimotor Cortex / Q000293:injuries / Q000473:pathology; D016708:Synaptophysin / Q000378:metabolism
D019922:GAP-43 Protein; D016708:Synaptophysin