Spinal Cord Injury (SCI) is still a devastating clinical problem with irreversible consequences leading to permanent functional loss and life time disability. This study was conducted to assess the healing effect of bone marrow-derived mesenchymal stem cells on locomotor function and changes of Tumor Necrosis Factor alpha (TNF-α) after SCI in mice. Forty two BALB/C mice were divided into 3 equal groups of control, SCI and treatment [transplantation of 5×10 4 Bone Marrow Stem Cells (BMSCs)]. The SCI was induced by compression for 2 min at T10 and injury bilaterally. The femoral and tibial bones were used for bone marrow isolation and culture was made using Dulbecco's Modified Eagle's Medium supplemented with fetal bovine serum, L-glutamine and penicillin/streptomycin. Cell morphology was evaluated in all passages. Characterization of BMSCs was conducted by reverse transcription polymerase chain reaction and by osteogenic differentiation of BMSCs. The ELISA was undertaken for TNF-α. Open field locomotion was evaluated by Toyama mouse score. The BMSCs were plastic adherent and fibroblastic spindle-shape. MSCs were positive for CD90 and negative for CD34 and CD45. Osteogenic differentiation was noticed when stained with alizarin red. The serum TNF-α level increased after 24 h, 3 and 5 weeks post-SCI and was time dependent. The neurological score significantly improved after 8 weeks after BMSC transplantation. Transplantation of BMSCs was shown to decrease the TNF-α level and inflammation in injured spinal cord and improve the neurological outcome. These findings can be added to the literature for reduction of inflammation in SCI and improvement of neurological outcome after transplantation of BMSCs.
Spinal cord injury (SCI) following traumatic events is associated with the limited therapeutic options and sever complications, which can be partly due to inflammatory response. Therefore, this s tudy aims to explore the role of inflammation in spinal cord injury. The findings showed that the pathological conditions of nervous sys tem lead to activation of microglia, as trocyte, neutrophil, and macrophages. It is also may be mediated by glial and lead to neuronal injury and death through production of proinflammatory factors, such as cytokines (key factors in the onset, progression and suppression of inflammation) and chemokines. Inflammation is a major component of spinal cord injury; although it is possible that inflammation has beneficial effects, such as phagocytosis of apoptotic cells and pathogens clearance. However, this could contribute to spreading, amplifying, and chronicity of tissue damage, via production of neurotoxic factors. Conclusion: It seems that inflammation has a major role in the injured spinal cord. Identifying effective cells in the inflammatory responses as well as their numbers, nature of their actions, and types of released inflammatory factors, along with the discovery of appropriate coping s trategies agains t them, will increase the hope to repair spinal cord injuries in future.
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