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首页> 外文期刊>European journal of paediatric neurology: EJPN : official journal of the European Paediatric Neurology Society >T3 replacement does not prevent excitotoxic cell death but reduces developmental neuronal apoptosis in newborn mice.
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T3 replacement does not prevent excitotoxic cell death but reduces developmental neuronal apoptosis in newborn mice.

机译：T3替代不能防止兴奋性毒性细胞死亡，但可以减少新生小鼠的发育神经元凋亡。

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BACKGROUND: Periventricular leukomalacia (PVL) is a major cause of neurological handicap in pre-term infants. At present, there are no effective or causal therapies available. Thyroid hormones play an essential role in brain development and are reported to be decreased in pre-terms and following brain injury in adults. HYPOTHESIS: Excitotoxic brain damage of newborn mice decreases thyroid hormone concentrations. Exogenous T3 administration restores thyroid hormone levels and reduces perinatal brain damage in an animal model of PVL. DESIGN AND METHOD: To create white and gray matter (WM/GM) lesion mimicking several key aspects of PVL, we injected ibotenic acid (Ibo), a glutamate analog, into the right hemisphere (intracranially (i.c.)) of 5-day-old mice. T3 (10 microg/kg body weight (bw)) was injected intraperitoneally (i.p.) 1 h or repeatedly 1/24/48/72/96 h post-insult. We determined lesion size, number of apoptotic cells in WM/GM and serum T3/T4 concentration at 24 and 120 h after injury. Serum T3/T4concentration was also determined before and 1 and 2h after T3 administration. RESULTS: Excitotoxic brain damage did not alter serum T3/T4 concentrations within 120 h of injury. Serum T3 levels were distinctly elevated within 1 h of T3 injection; however, this elevation was relatively short-lived (half-life estimated to be less than 12 h). Neither single nor repetitive T3 treatment regimen reduced excitotoxic lesion size, but it did reduce apoptosis. CONCLUSIONS: T3 replacement does not prevent excitotoxic cell death, but it does reduce developmental neuronal apoptosis, which could participate to the beneficial neuropsychological effects of hormone therapy. Further study is therefore warranted.
机译：背景：室周白细胞软化（PVL）是早产儿神经功能障碍的主要原因。当前，没有有效的或因果疗法。甲状腺激素在大脑发育中起着至关重要的作用，据报道在成人早产儿和脑损伤后甲状腺激素会减少。假设：新生小鼠的兴奋性脑损伤可降低甲状腺激素浓度。在PVL动物模型中，外源性T3给药可恢复甲状腺激素水平并减少围产期脑部损伤。设计与方法：要创建模仿PVL几个关键方面的白色和灰色物质（WM / GM）病变，我们在5天的右半球（颅内（ic））注射了谷氨酸类似物ibotenic acid（Ibo）。老老鼠。将T3（10微克/千克体重（bw））腹膜内（i.p.）注射1小时，或在受伤后重复1/24/48/72/96小时。我们确定了损伤后24和120 h的病变大小，WM / GM中的凋亡细胞数和血清T3 / T4浓度。还测定了在施用T3之前，之后1和2h的血清T3 / T4浓度。结果：兴奋性脑损伤未在受伤120小时内改变血清T3 / T4浓度。注射T1后1小时血清T3水平明显升高。然而，这种升高是相对短暂的（半衰期估计少于12小时）。单一或重复的T3治疗方案均未减少兴奋性毒性病变的大小，但确实减少了细胞凋亡。结论：T3替代不能预防兴奋性毒性细胞死亡，但可以减少发育性神经元凋亡，这可能参与激素治疗的有益神经心理作用。因此，有必要进一步研究。

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