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FeTPPS Reduces Secondary Damage and Improves Neurobehavioral Functions after Traumatic Brain Injury

机译:FeTPPS减少了颅脑外伤后的继发性损伤并改善了神经行为功能

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摘要

Traumatic brain injury (TBI) determinate a cascade of events that rapidly lead to neuron's damage and death. We already reported that administration of FeTPPS, a 5,10,15,20-tetrakis (4-sulfonatophenyl) porphyrin iron III chloride peroxynitrite decomposition catalyst, possessed evident neuroprotective effects in a experimental model of spinal cord damage. The present study evaluated the neuroprotective property of FeTPPS in TBI, using a clinically validated model of TBI, the controlled cortical impact injury (CCI). We observe that treatment with FeTPPS (30 mg/kg, i.p.) reduced: the state of brain inflammation and the tissue hurt (histological score), myeloperoxidase activity, nitric oxide production, glial fibrillary acidic protein (GFAP) and pro-inflammatory cytokines expression and apoptosis process. Moreover, treatment with FeTPPS re-established motor-cognitive function after CCI and it resulted in a reduction of lesion volumes. Our results established that FeTPPS treatment decreases the growth of inflammatory process and the tissue injury associated with TBI. Thus our study confirmed the neuroprotective role of FeTPPS treatment on TBI.
机译:颅脑外伤(TBI)决定了一系列事件,这些事件迅速导致神经元的损害和死亡。我们已经报道了FeTPPS(一种5,10,15,20-四(4-磺酰基苯基)卟啉铁III氯化物过氧亚硝酸盐分解催化剂)的给药在脊髓损伤的实验模型中具有明显的神经保护作用。本研究使用临床验证的TBI模型(可控制的皮质撞击损伤(CCI))评估了TTP中FeTPPS的神经保护特性。我们观察到FeTPPS(30 mg / kg,ip)的治疗降低了:脑部炎症和组织损伤的状态(组织学评分),髓过氧化物酶活性,一氧化氮生成,神经胶质原纤维酸性蛋白(GFAP)和促炎性细胞因子的表达和凋亡过程。此外,用FeTPPS进行治疗可在CCI后重新建立运动认知功能,并减少病变体积。我们的结果表明,FeTPPS治疗可减少炎症过程的增长以及与TBI相关的组织损伤。因此,我们的研究证实了FeTPPS治疗对TBI的神经保护作用。

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