Abstract
The present study investigates the effects of carnosine and/or cyclosporine A (CyA) treatment against traumatic brain injury (TBI) in immature rats. Traumatized rats received carnosine [(200 mg/kg/day, in pre-and post-treatment (i.p.)] for 7 consecutive days following TBI. CyA (20 mg/kg, i.p.) was administrated 15 min and 24 h after TBI. The results revealed that TBI caused sever brain injury indicated by increased nucleotide hydrolysis which was ensured by pronounced increase in ectonucleotidases, NTPDases (ATP and ADP hydrolysis) and 5'-nucleotidase (AMP hydrolysis) in traumatized rats compared with normal animals. TBI also causes elevation of glycolytic enzymatic activities as lactate dehydrogenase (LDH) and phosphoglucoisomerase (PGI) in rats’ brains. In addition TBI pronouncedly reduced the activities of antioxidant enzymes glutathione reductase (GR) and catalase (CAT) in brain tissue as compared to normal animals. Injection of carnosine and/or CyA significantly modulates the altered enzymatic activities. In conclusion, the present data may suggest the beneficial effect of carnosine and/or CyA in protection of brain tissues from disorders induced by traumatic injury. Key words: Carnosine, cyclosporine A, glutathione reductase, traumatic brain injury (TBI).
Highlights
Traumatic brain injury (TBI) is associated with costly health problems and high mortality and morbidity in previously healthy populations
Data are expressed as mean± SD of 6 rats in each group. 5'-nucleotidase, NTPDase(ADP) and NTPDase(ATP) enzyme activities are expressed as μmol Pi released/min/mg protein. aP< 0.0001, bP< 0.05 compared with normal control group. cP < 0.0001 when compared with TBI untreated group. n=non-significant when compared with normal group, using ANOVA followed by Bonferroni as post ANOVA test
Our results revealed that TBI pronouncedly reduced the activities of antioxidant enzymes, glutathione reductase (GR) and catalase (CAT), in rats’ brain relative to their level in normal animals
Summary
Traumatic brain injury (TBI) is associated with costly health problems and high mortality and morbidity in previously healthy populations. Despite advances in research and improved neurological intensive care in recent years, the clinical outcome of severely headinjured patients is still poor. Posttraumatic brain damage is determined by a combination of primary and secondary insults. Primary damage results from mechanical forces applied to the skull and brain at the time of impact, leading to focal or diffuse brain injury patterns. In contrast to the primary insult, secondary brain injuries evolve over time. These injuries are characterized by a complex cascade of molecular and biochemical events that lead to neuroinflammation, brain edema, and delayed neuronal death (Beauchamp et al, 2008)
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