Neuroprotective Effects of Bone Marrow Mesenchymal Stem Cells on Bilateral Common Carotid Arteries Occlusion Model of Cerebral Ischemia in Rat

Author:

Pourheydar Bagher12,Soleimani Asl Sara34ORCID,Azimzadeh Mostafa5,Rezaei Moghadam Adel6,Marzban Asghar7,Mehdizadeh Mehdi8ORCID

Affiliation:

1. Department of Anatomical Sciences, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran

2. Neurophysiology Research Center, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran

3. Anatomy Department, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran

4. Cell Therapy Division of Endometrium and Endometriosis Research Center, Hamadan University of Medical Sciences, Hamadan, Iran

5. Young Researchers and Elite Club, Islamic Azad University, Yazd Branch, Yazd, Iran

6. Faculty of Veterinary Medicine, Islamic Azad University, Tabriz Branch, Tabriz, Iran

7. Department of Pediatrics, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran

8. Cellular and Molecular Research Center, Department of Anatomy, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran

Abstract

Cell therapy is the most advanced treatment of the cerebral ischemia, nowadays. Herein, we discuss the neuroprotective effects of bone marrow mesenchymal stem cells (BMSCs) on rat hippocampal cells following intravenous injection of these cells in an ischemia-reperfusion model. Adult male Wistar rats were divided into 5 groups: control, sham (surgery without blockage of common carotid arteries), ischemia (common carotid arteries were blocked for 30 min prior to reperfusion), vehicle (7 days after ischemia PBS was injected via the tail vein), and treatment (injections of BMSC into the tail veins 7 days after ischemia). We performed neuromuscular and vestibulomotor function tests to assess behavioral function and, finally, brains were subjected to hematoxylin and eosin (H&E), anti-Brdu immunohistochemistry, and TUNEL staining. The ischemia group had severe apoptosis. The group treated with BMSCs had a lower mortality rate and also had significant improvement in functional recovery (P<0.001). Ischemia-reperfusion for 30 min causes damage and extensive neuronal death in the hippocampus, especially in CA1 and CA3 regions, leading to several functional and neurological deficits. In conclusion, intravenous injection of BMSCs can significantly decrease the number of apoptotic neurons and significantly improve functional recovery, which may be a beneficial treatment method for ischemic injuries.

Publisher

Hindawi Limited

Subject

Neurology (clinical),Neurology,General Medicine,Neuropsychology and Physiological Psychology

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