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Zhang, L., Schallert, T., Zhang, Z.G., Jiang, Q., Arniego, P., Li, Q., Lu, M. and Chopp, M. (2002) A Test for Detecting Long-Term Sensorimotor Dysfunction in the Mouse after Focal Cerebral Ischemia. Journal of Neuroscience Methods, 117, 207-214. http://dx.doi.org/10.1016/S0165-0270(02)00114-0

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• TITLE: Thymosin β4 Improves Neurological Outcome and Enhances Induced Oligodendrogenesis in the Rat after ICH

  AUTHORS: Dongmei Yang, Yuxia Han, Michael Chopp, Donald M. Seyfried

  KEYWORDS: Thymosin β4, Neurogenesis, Oligodendrogenesis, Intracerebral Hemorrhage

  JOURNAL NAME: World Journal of Neuroscience, Vol.4 No.5, October 23, 2014

  ABSTRACT: Thymosin β4 (Tβ4), a G-actin binding protein, has diverse biological functions. This study tested the effects of Tβ4 on oligodendrogenesis in a rat model of intracerebral hemorrhage (ICH). ICH was induced by stereotactic injection of 100 μm of autologous blood into the striatum in 32 male Wistar rats. The rats were randomly divided into four groups: 1) saline control group (n = 8); 2) 3 mg/kg Tβ4-treated group (n = 8); 3) 6 mg/kg Tβ4-treated group (n = 8); and 4) 12 mg/kg Tβ4treated group (n = 8). Tβ4 or saline was administered intraperitoneally starting at 24 h post ICH and then every 3 days for 4 additional doses. The neurological functional outcome was evaluated by behavioral tests (i.e., modified Neurological Severity Score and corner turn test) at multiple time points after ICH. Animals were sacrificed at 28 days post ICH, and histological studies were completed. Tβ4 treatment improved neurological functional recovery significantly and increased actively proliferating oligodendrocytic progenitor cells and myelinating oligodendrocytes in the ICH-affected brain tissue, compared with the saline-treated group. The high-dose treatment of Tβ4 showed better restorative effects compared with the low-dose treatment. Tβ4 treatment enhanced ICH-induced oligodendrogenesis that may contribute to the enhanced functional recovery after ICH. Further investigation is warranted to determine the associated underlying mechanisms of Tβ4 treatment for ICH.