Suppression of Neuroinflammation by Platelet-Rich Plasma Improves Functional Recovery in the Rat Model of Spinal Cord Injury

سال انتشار: 1398
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 451

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شناسه ملی سند علمی:

NIMED03_062

تاریخ نمایه سازی: 7 آبان 1398

چکیده مقاله:

Spinal cord injury (SCI) is serious damage with many clinical complications on patients. The pathophysiology of SCI involves a primarymechanical injury that is followed by a secondary phase. The inflammation is one of the most important processes in secondary injury. If inflammation is not controlled, it leads to expansion of the damage. Platelet-rich plasma (PRP) is an autologous blood-derived product. PRP isa key source of growth factors and anti-inflammatory ingredients involved in tissue repair and regeneration. Materials and Methods: Adult male Wistar rats (n=21) were assigned to 3 groups: control, SCI and SCI+PRP groups. The SCI was created at the T10 level. 10 μl PRP was injected intrathecally 24 hours after SCI. After 3 days the spinal cord samples were collected and the level of TNF-α, IL-1β, and IL-6 was measured. The Basso, Beattie, Bresnahan (BBB) locomotor rating scale was used at 1, 3, 7, 14, 21 and 28 days after SCI. Also, hematoxylin and eosin (H&E) staining was performed at day 28 for spinal cord tissue analysis. Results: The level of TNF-α, IL-1β, and IL-6 significantly increased after SCI. The level of these pro-inflammatory cytokines significantly decreased in the SCI+PRP group comparedwith the SCI group. In addition, the comparison between SCI and treatment groups determined a significant reduction in tissue degeneration and the volume of cavities in the SCI+PRP group. Also, BBB scores were significantly increased in PRP-treated rats on days 14, 21 and 28 after injury compared with the SCI group. Conclusion: By reducing the inflammation after SCI, PRP could prevent spinal cord degeneration and thedeath of neural cells and improve motor function in the rat. By conducting further studies, PRP can be a good option to regulate neuroinflammation.

نویسندگان

Morteza Gholaminejhad

Department of Anatomy, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Gholamreza Hassanzadeh

Department of Anatomy, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Ibrahim Mohammed

Department of Anatomy, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Mohammad Akbari

Department of Anatomy, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran