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

机译:FETPPS减少次要损伤并在创伤性脑损伤后改善神经兽性功能

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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:创伤性脑损伤(TBI)确定迅速导致神经元损害和死亡的级联事件。我们已经报道,施用FETPPS,5,10,15,20-四磺基苯基)卟啉铁III氯化物过氧腈分解催化剂,在脊髓损伤的实验模型中具有明显的神经保护作用。本研究评估了在TBI中使用临床验证的TBI,受控皮质冲击损伤(CCI)中TBI中的FETPPS的神经保护性能。我们观察到FetPPS的治疗(30mg / kg,IP)减少:脑炎症的状态和组织损伤(组织学评分),肌释放酶活性,一氧化氮产生,胶质纤维酸性蛋白(GFAP)和促炎细胞因子表达和凋亡过程。此外,在CCI之后用FETPPS重新建立电动机认知函数的处理,导致病变量减少。我们的结果确定,FETPPS处理降低了炎症过程的生长和与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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