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BackgroundPrematurebabies with periventricular white matter injury (PWMI) exhibit spastic motordeficits and cognitive or behavior deficits without effective treatment. Our invivo study highlighted the therapeutic role of thyroxin (T4) on PWMI. Wedemonstrated T4 post-treatment decreased pre-OLs proliferation and may drivethem toward maturation.To understand the maturational status, we analyzed the oligodendrocytesmaturation –dependent transcription factors after T4 treatment.Materials and MethodsA PWMI animal model wasestablished by unilateral carotid artery ligation followed by 6.5% 1 hour ofhyoxia (HI) in P7 rat pups. The pups were subjected to normal saline (NS), T4200μg/Kg (T4-0.2), and T41 mg/Kg (T4-1) after HI. At 96 hrs after HI, the cerebral white matter was dissected out for RNAextraction. Total RNA wereisolated from the white matter for quantitative real-time PCR. The following transcription factors were analyzed: PDGFα，SOX8，SOX10，Nkx2.2.Each sample was tested in triplicate and dataanalysis used the 2- ΔΔCT method. ResultsSOX10mRNA was up-regulated from P9 during immature brain development. PDGFα and SOX10 mRNA expression increased significantlyat 96 hrs after HI. T4 treatment after HI increased NKx2.2 mRNA expressioncompared with NS- and T4-0.2-treated rats.ConclusionSox10gene plays an important role during brain development in immature rat pups. HIincreases PDGFα mRNA expression may indicate replenishmentof pre-OLs in the white matter. T4 post-treatment after HI would up-regulateSOX10 and Nkx2.2 gene expression. The SOX10 and NKx2.2 genes are turned onafter T4 post-treatment in the rats with HI insult.