Abstract
Purpose To evaluate the neuroprotective effect of L-alanyl-glutamine in a gerbil model of brain ischemia-reperfusion injury based on immunohistochemical quantification of pro-inflammatory and cell activation biomarkers (TNF-α, NF-κB, IL-6 and HO-1).Methods Male gerbils weighing 100-180 g were pretreated with either 0.75 g/kg L-Ala-Gln (n=18) or 2.0 mL saline (n=18) administered i.v. 30 minutes before the bilateral ligation of the common carotid artery during 15 min and then the ligation was removed. Under anesthesia with urethane, brain tissue was harvested at 0 min (T0), 30 min (T30) and 60 min (T60) after reperfusion. The tissue was embedded in 10% formalin overnight and 4-μm sections were prepared for immunostaining with monoclonal antibodies. Immunostained cells were counted by optical microscopy. The statistical analysis used mean values based on 4 sections.Results The pretreatment with L-Ala-Gln animal group 1 demonstrated significantly lower levels of TNF-α, NF-κB and IL-6. On the other hand, the levels of HO-1 were significantly higher, suggesting a protective role in model of brain ischemia-reperfusion injury.Conclusion These findings suggest a protective effect of L-Ala-Gln by decreasing levels of TNF-alpha, IL-6 and NF-κB and Increasing levels of HO-1.
Highlights
Cerebrovascular diseases are currently the thirdmost important cause of death in several developed and developing countries
Reperfusion after brain ischemia increases the levels of pro-oxidant reactive oxygen species (ROS) in the brain tissue and may lead to neuronal injury as ROS interact directly with macromolecules or indirectly affect cellular signaling pathways and the regulation of gene expression[4]
The aim of this study was to evaluate the role of L-Ala-Gln to protect against brain ischemia-reperfusion injury in a gerbil model evaluated through immunohistochemistry (IHC) for the IL-6, TNF-α, NF-κB and heme oxygenase-1 (HO-1)
Summary
Cerebrovascular diseases are currently the thirdmost important cause of death in several developed and developing countries. According to the National Institute of Health, cerebrovascular diseases affect about 500,000 people every year in the U.S, with a mortality rate of 20-30% and a similar rate of severe disability[2]. Cerebral ischemia is a reduction or total absence of oxygen and other metabolic substrates in the brain due to total or partial obstruction of the blood supply[3]. Reperfusion after brain ischemia increases the levels of pro-oxidant reactive oxygen species (ROS) in the brain tissue and may lead to neuronal injury as ROS interact directly with macromolecules (including proteins, lipids and DNA) or indirectly affect cellular signaling pathways and the regulation of gene expression[4]. IL-6 is a cytokine and its physiological role in injury-induced inflammation shows a potent pro-inflammatory role[7]
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