The effect of Hippophae rhamnoides L. Extract on acrylamide-induced brain injury in rats

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Turan M. I., Aktaş M., Gündoğdu B., Karahan Yilmaz S., Süleyman H.

Acta Cirurgica Brasileira, vol.36, no.10, 2021 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 36 Issue: 10
  • Publication Date: 2021
  • Doi Number: 10.1590/acb361005
  • Journal Name: Acta Cirurgica Brasileira
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED)
  • Keywords: Hippophae, Acrylamide, Brain Injuries, Toxicity, Rats
  • Erzincan Binali Yildirim University Affiliated: Yes


© 2021, Sociedade Brasileira para o Desenvolvimento de Pesquisa em Cirurgia. All rights reserved.Purpose: Reactive oxygen species (ROS), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) have been shown in the pathogenesis of acrylamide neurotoxicity. Hippophae rhamnoides L. extract (HRE) has a cytoprotective effect by stabilizing the production of ROS, IL-1β and TNF-α. The objective of the article was to investigate the effect of HRE on acrylamide-induced brain damage in rats biochemically and histopathologically. Methods: To the HRE+acrylamide only (ACR) group (n=6) of the animals, HRE was administered orally at a dose of 50 mg / kg into the stomach by gavage. The same volume of solvent (olive oil) was administered orally to the ACR (n=6) and healthy (HG) (n=6) groups. One hour after HRE administration, acrylamide was given orally at a dose of 20 mg/kg to HRE+ACR and ACR groups in the same way. This procedure was repeated once a day for 30 days. At the end of this period, brain tissues extracted from animals killed with 50 mg/kg thiopental anesthesia were examined biochemically and histopathologically. Results: It has been shown that HRE prevents the increase of malondialdehyde (MDA), myeloperoxidase (MPO), IL-1β and TNF-α with acrylamide and the decrease of total glutathione (tGSH) and glutathione reductase (GSHRd) levels in brain tissue. Conclusion: HRE may be useful in the treatment of acrylamide-induced neurotoxicity.