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首页> 外文期刊>BMC Neuroscience >The neuroprotective effects of AMN082 on neuronal apoptosis in rats after traumatic brain injury
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The neuroprotective effects of AMN082 on neuronal apoptosis in rats after traumatic brain injury

机译：AMN082对创伤性脑损伤后大鼠神经元细胞凋亡的神经保护作用

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The aim of this study was to investigate whether AMN082 exerts its neuroprotective effect by attenuating glutamate receptor-associated neuronal apoptosis and improving functional outcomes after traumatic brain injury (TBI). Anesthetized male Sprague–Dawley rats were divided into the sham-operated, TBI? ?vehicle, and TBI? ?AMN082 groups. AMN082 (10?mg/kg) was intraperitoneally injected 0, 24, or 48?h after TBI. In the 120?min after TBI, heart rate, mean arterial pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) were continuously measured. Motor function, the infarct volume, neuronal nitrosative stress-associated apoptosis, and N-methyl-d-aspartate receptor 2A (NR2A) and NR2B expression in the pericontusional cortex were measured on the 3rd day after TBI. The results showed that the AMN082-treated group had a lower ICP and higher CPP after TBI. TBI-induced motor deficits, the increase in infarct volume, neuronal apoptosis, and 3-nitrotyrosine and inducible nitric oxide synthase expression in the pericontusional cortex were significantly improved by AMN082 therapy. Simultaneously, AMN082 increased NR2A and NR2B expression in neuronal cells. We concluded that intraperitoneal injection of AMN082 for 3?days may ameliorate TBI by attenuating glutamate receptor-associated nitrosative stress and neuronal apoptosis in the pericontusional cortex. We suggest that AMN082 administration in the acute stage may be a promising strategy for TBI.
机译：本研究的目的是研究AMN082是否通过衰减谷氨酸受体相关的神经元细胞凋亡并在创伤后脑损伤（TBI）后改善功能性结果来施加其神经保护作用。麻醉的雄性Sprague-Dawley大鼠分为假手术，TBI？ ？车辆和TBI？ ？AMN082组。在TBI之后，AMN082（10？Mg / kg）腹膜内注射0,24或48℃。在TBI，心率，平均动脉压，颅内压（ICP）和脑灌注压力（CPP）之后，在120℃下进行连续测量。在TBI后的第3天测量在TBI后的第3天测量在第3天测定在第3天测定骨密化皮质中的梗塞体积，神经元亚硝基胁迫相关的凋亡和N-甲基-D-天冬氨酸受体2a（nR2a）和NR2b表达。结果表明，在TBI后，AM082治疗组的ICP和更高的CPP。 TBI诱导的电动机缺陷，梗塞体积，神经元细胞凋亡和3-硝基荧光蛋白和诱导的一氧化氮合酶和诱导的一氧化氮合酶表达，通过AMN082疗法显着改善。同时，AM082增加了神经元细胞中的NR2A和NR2B表达。我们得出结论，腹膜内注射AM082的3？天可以通过衰减谷氨酸受体相关的亚硝化胁迫和神经细胞凋亡在细胞统计皮层中来改善TBI。我们建议在急性阶段的AM082管理可能是TBI的有希望的策略。

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