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首页> 外文期刊>Chinese Journal of Traumatology >Changes of metabotropic glutamate receptor subtype 1 a in diffuse brain injury with secondary brain insults and the effects of 2-methyl-4-carboxyphenylglycine
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Changes of metabotropic glutamate receptor subtype 1 a in diffuse brain injury with secondary brain insults and the effects of 2-methyl-4-carboxyphenylglycine

机译:继发性脑损伤在弥漫性脑损伤中代谢型谷氨酸受体亚型1a的变化及2-甲基-4-羧苯基甘氨酸的作用

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摘要

Objective: To observe the changes of metabotropic glutamate receptor la in rat brain in a rodent model of diffuse head injury with secondary insults and the effects of 2-methyl-4-carboxyphenylglycine (MCPG). Methods: Based on Marmarous rodent model of diffuse brain injury ( DBI), hypotension was made by blood withdrawal as secondary brain insults (SBI). 105 male SD rats were randomized into A and B groups. The changes of mGluR_(1a) in cerebral cortex were studied by immunohistochemistry and the effect of MCPG by HE. Each group was divided into different subgroups at different time after injury. Results: Compared with that of sham group, the number of mGluR_(1a) positive neuron increased by 12.9 +-3.2 (P<0.05) 1 day after injury in the injured cerebral cortex in DBI group. However, in DBI and SBI group there was a more significant increase in the number of mGluR_(1a) positive neuron at 4 hours after injury (15.6 +-3.0, P < 0.05) and then the number of mGluR_(1a) positive neuron gradually decreased. Administration of MCPG reduced total cortical necrotic neurons counts on the 7th day after injury (5.21 +-2.52, P<0.05). Conclusions: Brain injury can increase the gene expression of mGluR_(1a) and the role of mGluR_(1a) may be a key factor in the aggravation of head injury with SBI, and that MCPG may have therapeutic potential in head injury.
机译:目的:观察在患有继发性伤害的弥漫性颅脑损伤的啮齿动物模型中大鼠代谢型谷氨酸受体la的变化以及2-甲基-4-羧苯基甘氨酸(MCPG)的作用。方法:基于Marmarous弥漫性脑损伤的啮齿动物模型(DBI),通过抽血作为继发性脑损伤(SBI)来降低血压。将105只雄性SD大鼠随机分为A组和B组。免疫组织化学研究了大脑皮层mGluR_(1a)的变化,HE观察了MCPG的作用。每组在受伤后的不同时间分为不同的亚组。结果:与假手术组相比,DBI组受伤后1天,mGluR_(1a)阳性神经元数目增加了12.9±-3.2(P <0.05)。然而,在DBI和SBI组中,在损伤后4小时,mGluR_(1a)阳性神经元的数量显着增加(15.6 + -3.0,P <0.05),然后逐渐增加。减少。损伤后第7天,MCPG的施用减少了总的皮质坏死神经元计数(5.21 + -2.52,P <0.05)。结论:脑损伤可增加mGluR_(1a)的基因表达,mGluR_(1a)的作用可能是SBI加重颅脑损伤的关键因素,MCPG在颅脑损伤中可能具有治疗潜力。

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