ABSTRACT
Introduction: Traumatic brain injury (TBI) remains a leading cause of disability and death among young people in China. Unfortunately, no specific pharmacological agents to block the progression of secondary brain injury have been approved for clinical treatment. Recently, neuroprotective effects of erythropoietin (EPO) have been demonstrated in addition to its principal function in erythropoiesis, and hence it is viewed as a potential drug for TBI. In this study, we have investigated the neuroprotective effects of EPO associated with immune/inflammatory modulation in a mouse experimental TBI model. Methods: EPO (5000 U/kg body weight, i.p.) was injected at 1 hr, 1, 2, and 3 days after TBI, and its effect on cognitive function, brain edema, immune/inflammatory cells including regulatory T cells (Tregs), neutrophils, CD3+ T cells, and microglia, cytokines including interleukin-10 (IL-10), transforming growth factor-ß (TGF-ß), interleukin-1ß (IL-1ß), and tumor necrosis factor-α (TNF-α) were evaluated at different time points after treatment. Results: EPO treatment significantly decreased brain edema and improved cognitive function when compared to Saline-treated mice (p < .05). EPO treatment also significantly increased Tregs level in spleen and injured brain tissue as well as significantly reduced the infiltration and activation of immune/inflammatory cells (neutrophils, CD3+T cells, and microglia) in the injured hemisphere compared to Saline-treated control animals (p < .05). In addition, ELISA analysis demonstrated that EPO treatment increased the expression of anti-inflammatory cytokine IL-10, but decreased the expression of proinflammatory cytokine IL-1ß and TNF-α in the injured brain tissue (p < .05). Conclusions: These findings suggest that EPO could improve neurological and cognitive functional outcomes as well as regulate immune/inflammatory reaction in TBI.
Subject(s)
Brain Edema/drug therapy , Brain Injuries, Traumatic , Cognition/drug effects , Erythropoietin/pharmacology , Animals , Brain/drug effects , Brain/physiopathology , Brain Injuries, Traumatic/drug therapy , Brain Injuries, Traumatic/immunology , Disease Models, Animal , Inflammation/drug therapy , Interleukin-1beta/analysis , Male , Mice , Neuroprotective Agents/pharmacology , Treatment Outcome , Tumor Necrosis Factor-alpha/analysisABSTRACT
To lower the overpotential of a lithium-oxygen battery, electron transport at the solid-to-solid interface between the discharge product Li2O2 and the cathode catalyst is of great significance. Here we propose a strategy to enhance electron transport property of the cathode catalyst by the replace of oxygen atoms in the generally used metal oxide-based catalysts with nitrogen atoms to improve electron density at Fermi energy after nitridation. Hierarchically porous CoN nanorods were obtained by thermal treatment of Co3O4 nanorods under ammonia atmosphere at 350 °C. Compared with that of the pristine Co3O4 precursor before nitridation, the overpotential of the obtained CoN cathode was significantly decreased. Moreover, specific capacity and cycling stability of the CoN nanorods were enhanced. It is assumed that the discharged products with different morphologies for Co3O4 and CoN cathodes might be closely associated with the variation in the electronic density induced by occupancy of nitrogen atoms into interstitial sites of metal lattice after nitridation. The nitridation strategy for improved electron density proposed in this work is proved to be a simple but efficient way to improve the electrochemical performance of metal oxide based cathodes for lithium-oxygen batteries.
