Document Type : Original Article
Authors
1
Department of Anatomy, Faculty of Medicine, Uhanto University, Kabol, Afghanestan
2
Cellular and Molecular Research Center, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran;Department of Anatomy, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
3
4Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran;5Department of Anatomy, Faculty of Medicine, Hamadan University of Medical Sciences Hamadan, Iran
4
6Neurophysiology Research Center, Department of Anatomy, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
5
4Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
6
Department of Anatomy, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran;7Cellular and Molecular Research Center, Faculty of Advanced Technologies in Medicine, Department of Anatomy, Iran University
Abstract
Objective
Stroke is most important cause of death and disability in adults. The hippocampal CA1 and sub-ventricular zone neurons are vulnerable to ischemia that can impair memory and learning functions. Although neurogenesis normally occurs in the dentate gyrus (DG) of the hippocampus and sub-ventricular zone (SVZ) following brain damage, this response is unable to compensate for severely damaged areas. This study aims to assess both neurogenesis and the neuroprotective effects of transforming growth factor-alpha (TGF-α) on the hippocampus and SVZ following ischemia-reperfusion.
Materials and Methods
In this experimental study, a total of 48 male Wistar rats were divided into the following groups: surgical (n=12), phosphate buffered saline (PBS) treated vehicle shams (n=12), ischemia (n=12) and treatment (n=12) groups. Ischemia was induced by common carotid occlusion for 30 minutes followed by reperfusion, and TGF-α was then injected into the right lateral ventricle. Spatial memory was assessed using Morris water maze (MWM). Nestin and Bcl-2 family protein expressions were studied by immunohistochemistry (IHC) and Western blot methods, respectively. Finally, data were analyzed using Statistical Package for the Social Sciences (SPSS, SPSS Inc., Chicago, USA) version 16 and one-way analysis of variance (ANOVA).
Results
TGF-α injection significantly increased nestin expression in both the hippocampal DG and SVZ areas. TGF-α treatment caused a significant decrease in Bax expression and an increase in Bcl-2 anti-apoptotic protein expression in the hippocampus. Our results showed a significant increase in the number of pyramidal neurons. Memory also improved significantly following TGF-α treatment.
Conclusion
Our findings proved that TGF-α reduced ischemic injury and played a neuroprotective role in the pathogenesis of ischemic injury.
Keywords
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