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BACKGROUND:Transplantation of bone marrow-derived mesenchymal stem cells(BMSCs) improves motor functional recovery,but the mechanisms remain unclear.OBJECTIVE:To investigate expression of growth-associated protein 43(GAP-43) and neural cell adhesion molecule following BMSC transplantation to the lateral ventricle in rats with acute focal cerebral ischemic brain damage.DESIGN,TIME AND SETTING:A randomized,controlled,animal experiment using immunohistochemistry was performed at the laboratories of Department of Neurology,Renmin Hospital of Wuhan University and Doctoral Scientific Research Work Station of C-BONS PHARMA,Hubei Province,China,from January 2007 to December 2008.MATERIALS:Monoclonal mouse anti-rat 5-bromo-2-deoxyuridine and neural cell adhesion molecule antibodies were purchased from Sigma,USA;monoclonal mouse anti-rat GAP-43 antibody was purchased from Wuhan Boster,China.METHODS:Rat models of right middle cerebral artery occlusion were established using the thread method.At 1 day after middle cerebral artery occlusion,20 μL culture solution,containing 5 × 105 BMSCs,was transplanted to the left lateral ventricle using micro-injection.MAIN OUTCOME MEASURES:Scores of neurological impairment were measured to assess neural function.Expression of GAP-43 and neural cell adhesion molecule at the lesion areas was examined by immunohistochemistry.RESULTS:GAP-43 and neural cell adhesion molecule expression was low in brain tissues of the sham-operated group,but expression increased at the ischemic boundary(P < 0.05).Transplantation of BMSCs further enhanced expression of GAP-43 and neural cell adhesion molecule(P < 0.05) and remarkably improved neurological impairment of ischemic rats(P < 0.05).CONCLUSION:BMSC transplantation promoted neurological recovery in rats by upregulating expression of GAP-43 and neural cell adhesion molecule.
BACKGROUND: Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) improves motor functional recovery, but the mechanisms remain unclear. OBJECTIVE: To investigate expression of growth-associated protein 43 (GAP-43) and neural cell adhesion molecule following BMSC transplantation to the lateral ventricle in rats with acute focal cerebral ischemic brain damage. DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment using immunohistochemistry was performed at the laboratories of Department of Neurology, Renmin Hospital of Wuhan University and Doctoral Scientific Research Work Station of C-BONS PHARMA, Hubei Province, China, from January 2007 to December 2008. MIALIALS: Monoclonal mouse anti-rat 5-bromo-2-deoxyuridine and neural cell adhesion molecule antibodies were purchased from Sigma, USA; -43 antibody was purchased from Wuhan Boster, China. METHODS: Rat models of right middle cerebral artery occlusion were established using the thread method. At 1 day after middle cerebral artery occlusion, 20 μL culture solution containing 5 × 10 5 BMSCs, was transplanted to the left lateral ventricle using micro-injection. MAIN OUTCOME MEASURES: Scores of neurological impairment were measured to assess neural function. Expression of GAP-43 and neural cell adhesion molecule at the lesion areas was examined by immunohistochemistry .RESULTS: GAP-43 and neural cell adhesion molecule expression was low in brain tissues of the sham-operated group, but expression increased at the ischemic boundary (P <0.05). Transplantation of BMSCs further enhanced expression of GAP-43 and neural cell adhesion molecule (P <0.05) and remarkably improved neurological impairment of ischemic rats (P <0.05) .CONCLUSION: BMSC promoted promoted neurological recovery in rats by upregulating expression of GAP-43 and neural cell adhesion molecule.