Abstract
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.
Highlights
Traumatic brain injury (TBI) is a common problem that lead permanent disability in patients, in the developed countries (Finnie and Blumbergs, 2002)
The present study evaluated the neuroprotective property of FeTPPS in TBI, using a clinically validated model of TBI, the controlled cortical impact injury (CCI)
It has been suggested that reactive oxygen species (ROS) generation is activated at the lesion area after TBI, leading to the initial production of superoxide (O−2 ) and nitric oxide (NO) radicals (Schiavone and Trabace, 2016)
Summary
Traumatic brain injury (TBI) is a common problem that lead permanent disability in patients, in the developed countries (Finnie and Blumbergs, 2002). Diverse studies have reported that certain water-soluble iron (III) porphyry’s are highly active ONOO− decomposition catalysts, catalyzing the isomerization of ONOO− almost exclusively to nitrate producing the development of oxidizing radical species and nontoxic nitrate anion (Misko et al, 1998; Salvemini et al, 1998a). We examined ONOO− role in TBI using the ONOO− decomposition catalyst 5,10,15,20-tetrakis (4-sulfonatophenyl) porphyrin iron III chloride (FeTPPS) This compound, in physiologically relevant conditions, catalyzes rapid isomerization of ONOO− to nitrate (NO−3 ), its cytoprotective actions of FeTPPS were already observed in other studies (Salvemini et al, 1998a; Jensen and Riley, 2002). We would like to demonstrate, using this catalyst, that ONOO− possess a main part in the modulation of the secondary mechanism associated to TBI
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