Mesenchymal stem cell therapy improves erectile dysfunction in experimental spinal cord injury


Albayrak Ö., Şener T. E., Erşahin M., Özbaş-Turan S., Ekentok C., Tavukçu H., ...Daha Fazla

INTERNATIONAL JOURNAL OF IMPOTENCE RESEARCH, cilt.32, sa.3, ss.308-316, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 32 Sayı: 3
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1038/s41443-019-0168-1
  • Dergi Adı: INTERNATIONAL JOURNAL OF IMPOTENCE RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Abstracts in Social Gerontology, EMBASE, Gender Studies Database, MEDLINE
  • Sayfa Sayıları: ss.308-316
  • Marmara Üniversitesi Adresli: Evet

Özet

The aim of this study is to investigate the therapeutic potential of adipose-derived mesenchymal stem cell (AD-MSC) from brown adipose tissue on erectile dysfunction (ED) in experimentally induced spinal cord injury in rats. 24 male Wistar rats were divided into 3 groups; control, spinal cord injury (SCI) + vehicle, and SCI + AD-MSC. To induce SCI, a standard weight-drop method that induced a moderate to severe injury (100 g/cm force) at T7-T10, was used. AD-MSC (3 x 105 cells /5 mu L) was applied by local transplantation into the region of injury. At the end of four-weeks, rats underwent neurological examinations and then intracavernosal and mean arterial pressures (ICP and MAP) measurements. After decapitation, spinal cord and cavernosal tissue samples were taken to analyze neuronal nitric oxide synthase (n-NOS), proto-oncogene protein c-FOS and nerve growth factor (NGF). Tissues were also examined histologically. Spinal cord injury caused decrease on NGF and n-NOS levels while c-FOS was increased. The ICP/MAP value in vehicle-treated SCI rats was found to be significantly higher than the control group. On the other hand, in SCI + AD-MSC group, all these parameters were reversed back to control levels. AD-MSC therapy may be beneficial against erectile dysfunction in experimentally induced SCI by ameliorating neuronal damage.