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首页> 外文期刊>BMC Neuroscience >Retroviral expression of human arginine decarboxylase reduces oxidative stress injury in mouse cortical astrocytes
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Retroviral expression of human arginine decarboxylase reduces oxidative stress injury in mouse cortical astrocytes

机译：人精氨酸脱羧酶的逆转录病毒表达减少了小鼠皮质星形胶质细胞的氧化应激损伤

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Background In physiologic and pathologic conditions of the central nervous system (CNS), astrocytes are a double-edged sword. They not only support neuronal homeostasis but also contribute to increases in neuronal demise. A large body of experimental evidence has shown that impaired astrocytes play crucial roles in the pathologic process of cerebral ischemia; therefore, astrocytes may represent a breakthrough target for neuroprotective therapeutic strategies. Agmatine, an endogenous polyamine catalyzed from L-arginine by arginine decarboxylase (ADC), is a neuromodulator and it protects neurons/glia against various injuries. Results In this investigation, agmatine-producing mouse cortical astrocytes were developed through transduction of the human ADC gene. Cells were exposed to oxygen-glucose deprivation (OGD) and restored to a normoxic glucose-supplied condition. Intracellular levels of agmatine were measured by high performance liquid chromatography. Cell viability was evaluated by Hoechest/propidium iodide nuclear staining and lactate dehydrogenase assay. Expression of inducible nitric oxide synthase (iNOS) and matrix metalloproteinase s (MMPs) were assessed by a reverse transcription polymerase chain reaction, Western immunoblots, and immunofluorescence. We confirmed that ADC gene-expressed astrocytes produce a great amount of agmatine. These cells were highly resistant to not only OGD but also restoration, which mimicked ischemia-reperfusion injury in vivo . The neuroprotective effects of ADC seemed to be related to its ability to attenuate expression of iNOS and MMPs. Conclusion Our findings imply that astrocytes can be reinforced against oxidative stress by endogenous agmatine production through ADC gene transduction. The results of this study provide new insights that may lead to novel therapeutic approaches to reduce cerebral ischemic injuries.
机译：背景技术在中枢神经系统（CNS）的生理和病理状况中，星形胶质细胞是一把双刃剑。它们不仅支持神经元稳态，而且还有助于神经元死亡的增加。大量的实验证据表明，受损的星形胶质细胞在脑缺血的病理过程中起着至关重要的作用。因此，星形胶质细胞可能代表神经保护性治疗策略的突破性目标。胍丁胺是精氨酸脱羧酶（ADC）从L-精氨酸催化的内源性多胺，是一种神经调节剂，可保护神经元/神经胶质细胞免受各种伤害。结果在这项研究中，通过转导人ADC基因产生了产生胍基丁胺的小鼠皮质星形胶质细胞。将细胞暴露于氧葡萄糖剥夺（OGD），并恢复至常氧葡萄糖提供的状态。用高效液相色谱法测定细胞内胍丁胺的水平。通过Hoechest /碘化丙啶核染色和乳酸脱氢酶测定法评估细胞活力。通过逆转录聚合酶链反应，Western免疫印迹和免疫荧光评估诱导型一氧化氮合酶（iNOS）和基质金属蛋白酶（MMPs）的表达。我们证实，表达ADC基因的星形胶质细胞产生大量的胍丁胺。这些细胞不仅对OGD具有很高的抵抗力，而且对恢复具有很高的抵抗力，可以模拟体内的缺血再灌注损伤。 ADC的神经保护作用似乎与其减弱iNOS和MMPs表达的能力有关。结论我们的发现暗示星形胶质细胞可以通过ADC基因转导产生内源性胍丁胺而增强抗氧化应激能力。这项研究的结果提供了新的见解，可能会导致减少脑缺血损伤的新型治疗方法。

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