Does Decorin Protect Neuronal Tissue via Its Antioxidant and Antiinflammatory Activity from Traumatic Brain Injury: An Experimental Study

Abstract Background The development of secondary brain injury via oxidative stress after traumatic brain injury (TBI) is well known. Decorin inactivates Transforming growth factor-β1 (TGF-β1), complement system (CS) and Tumor necrosis factor-α (TNF-α) which are related the oxidative stress and apoptosis. Consequently, the aim of the present study was to evaluate the role of Decorin (DC) on TBI. Methods A total of 24 male rats were used and divided into four groups as follows; control, trauma, DC, and methylprednisolone (MP). The trauma, DC and MP groups were subjected to closed-head contusive weight-drop injuries. Rats received treatment with intraperitoneally (IP) saline, DC or MP respectively. All the animals were sacrificed at the 24th hour after trauma and brain tissues were extracted. The oxidant/antioxidant parameters [malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), nitric oxide (NO)] and caspase-3 in the cerebral tissue were analyzed, and histomorphological evaluation of the cerebral tissue was performed. Results Levels of MDA, NO and activity of caspase-3 were significantly reduced, in addition GPx and SOD levels were increased in the DC and MP groups when compared to the trauma group. The pathology scores and the percentage of degenerated neurons were statistically lower in the DC and MP groups than the trauma group. Conclusion The results of the present study showed that decorine inactivates TGF-β1 and protects the brain tissue and neuronal cells after TBI.