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首页> 外文期刊>International Journal of Clinical and Experimental Pathology >MiR-124 effect in neurons apoptosis in newborn rat with thyroid hypofunction
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MiR-124 effect in neurons apoptosis in newborn rat with thyroid hypofunction

机译：MiR-124对甲状腺功能低下新生大鼠神经元凋亡的影响

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摘要

Congenital thyroid hypofunction can cause a variety of developmental disorders. Hippocampus is an important structure participating in the cognitive activities. Neural function damage is able to induce hippocampal neuron apoptosis. As a miRNA expressed specifically and abundantly in brain tissue, miR-124 has protective effect to neuron apoptosis caused by cerebral apoplexy. However, its role in neuron apoptosis caused by thyroid hypofunction is still unclear. The rats were divided into four groups including normal group, thyroid hypofunction group, miR-124 negative control group, and miR-124 mimics group. Propylthiouracil (50 mg/d) was injected to the stomach to the rats with 15 d pregnancy till the newborn rats were born. Inducing the thyroid hypofunction rat model and then injecting miR-124 mimics to ventricle. Serum TSH, FT3 and FT4 were detected to confirm the model. Immunohistochemistry was carried out to calculate neuron number. Tunel assay was used to detect neuron apoptosis. Western blot was applied to detect apoptosis related protein Caspase-3, Bcl-2 and Bax expression. After brain injection miR-124 mimics, hippocampal neuron number and morphology both improved in 15 d newborn mice compared with thyroid hypofunction group. Tunel staining found positive neurons reduced, which indicated that miR-124 can inhibit hippocampal neuron apoptosis in thyroid hypofunction rats. Further Western blot results revealed that apoptosis inhibition might be related to down-regulating activated Caspase-3 and Bax levels, and up-regulating tumor-suppressor gene Bcl-2 expression. MiR-124 can protect neuron apoptosis in thyroid hypofunction rat.
机译：先天性甲状腺功能低下可引起多种发育障碍。海马是参与认知活动的重要结构。神经功能损伤能够诱导海马神经元凋亡。 miR-124作为一种在脑组织中特异性和丰富表达的miRNA，对由脑中风引起的神经元凋亡具有保护作用。然而，其在甲状腺功能低下引起的神经元凋亡中的作用仍不清楚。将大鼠分为正常组，甲状腺功能减退组，miR-124阴性对照组和miR-124模拟组四组。妊娠15天的大鼠向胃中注射丙硫氧嘧啶（50 mg / d），直至新生大鼠出生。诱导甲状腺功能低下的大鼠模型，然后将miR-124模拟物注入心室。检测血清TSH，FT3和FT4以证实模型。进行免疫组织化学计算神经元数目。 Tunel分析用于检测神经元凋亡。免疫印迹用于检测凋亡相关蛋白Caspase-3，Bcl-2和Bax的表达。与甲状腺功能低下组相比，脑部注射miR-124模拟后，15 d新生小鼠的海马神经元数量和形态均得到改善。 Tunel染色发现阳性神经元减少，这表明miR-124可以抑制甲状腺功能低下大鼠海马神经元的凋亡。进一步的蛋白质印迹结果表明，凋亡抑制可能与下调激活的Caspase-3和Bax的水平，以及上调肿瘤抑制基因Bcl-2的表达有关。 MiR-124可以保护甲状腺功能低下大鼠的神经元凋亡。

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