Neuroprotective effects of adrenomedullin in experimental traumatic brain injury model in rats

Ulus Travma Acil Cerrahi Derg. 2022 Jun;28(6):736-742. doi: 10.14744/tjtes.2021.01954.

Abstract

Background: Traumatic brain injuries cause damages in the brain in several ways, which include cell death because of edema, disruption of the blood-brain barrier, shear stress, and ischemia. In this study, we investigated the effects of adrenomedullin (AM) on oxidative stress and inflammation after head traumas in a rat model.

Methods: Eighteen male adult Wistar albino rats were randomized into three groups (n=6). No traumas were applied to the con-trol (C) group. Traumas were applied in line with Marmarau trauma model in the trauma group. The rats in the AM treatment group were treated with post-traumatic 12 μg/kg i.p. AM in addition to the trauma group. The rats were followed for 7 days in all groups and were then sacrificed. Brain tissues and blood samples were taken.

Results: In the trauma group, both tissue and serum MDA, TNF-α, and IL-6 levels were significantly increased compared to the control group (p<0.05). In the AM-treated group, serum TNF-α levels were significantly decreased compared to the trauma group (p<0.05). In the trauma group, both tissue and serum GSH levels were significantly decreased compared to the control group (p<0.05). In the trauma group, serum Vitamin D3 levels were significantly decreased compared to the control group (p<0.05). In the AM-treated group, both tissue and serum GSH levels were significantly increased compared to the trauma group (p<0.05).

Conclusion: These results indicate that AM has neuroprotective effects on traumatic brain injury in a rat model.

MeSH terms

  • Adrenomedullin / pharmacology
  • Animals
  • Brain Injuries*
  • Brain Injuries, Traumatic* / drug therapy
  • Male
  • Neuroprotective Agents* / pharmacology
  • Rats
  • Rats, Wistar
  • Tumor Necrosis Factor-alpha

Substances

  • Neuroprotective Agents
  • Tumor Necrosis Factor-alpha
  • Adrenomedullin