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BACKGROUND: The transcription factor Olig1 is required for oligodendrocyte maturation and demyelinated lesion repair, and is a key regulator of myelinogenesis following ischemia.OBJECTIVE: To examine the efficacy of intraventricular injection of a recombinant adenovirus-expressing Olig1 gene (Ad5-Olig1-eGFP) on oligodendrocyte maturation and myelin repair following focal cerebral ischemia.DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the Department of Neurology, Beijing Friendship Hospital Affiliated to Capital Medical University from January 2007 to March 2008.MATERIALS: Adenovirus and a recombinant adenovirus containing Olig1 gene (Ad5-Olig1) were provided by Vector Gene Technology, China.METHODS: All 50 rats were induced by middle cerebral artery occlusion. A total of 46 rats were successfully induced and were subsequently randomly assigned to a adenovirus (Ad5) group and a recombinant adenovirus-expression Olig1 gene (Ad5-Olig1) group, with 23 rats per group. One day after middle cerebral artery occlusion, either Ad5-Olig1-eGFP or Ad5-eGFP (10 μL, 2.3 × 10~(11)/mL) was injected into the lateral ventricle on the ischemic hemisphere. MAIN OUTCOME MEASURES: Adenovirus-mediated Olig1 gene expression in vitro and in vivo was measured by reverse transcription-polymerase chain reaction and immunofluorescence, respectively. Myelin basic protein (MBP) levels were evaluated by Western Blot, immunostaining, and electron microscopy. RESULTS: Exogenous Olig1 expression was measured at the periventricular zone of the lateral ventricle 1 day after Ad5-Olig1 injection. In the Ad5-Olig1-treated group, MBP protein levels and average intensity of MBP-immunoreactivity (-ir) increased 28 days after middle cerebral artery occlusion, compared with the control group (P < 0.01, P < 0.05). Furthermore, myelinated axonal numbers markedly increased following Ad5-Olig1 treatment.CONCLUSION: The present data suggested that Ad5-Olig1 gene therapy increased MBP expression and the number of remyelinating axons following cerebral ischemia.