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

Turan M. I., Gundogdu B., Yilmaz S. K., Suleyman H., Aktas M.

ACTA CIRURGICA BRASILEIRA, cilt.36, sa.10, 2021 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 36 Sayı: 10
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1590/acb361005
  • Dergi Adı: ACTA CIRURGICA BRASILEIRA
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database, Directory of Open Access Journals
  • Anahtar Kelimeler: Hippophae, Acrylamide, Brain Injuries, Toxicity, Rats, OXIDATIVE STRESS, NEUROTOXICITY, INFLAMMATION, ANTIOXIDANT, ANGIOGENESIS, GLYCIDAMIDE, TOXICITY, ENZYMES
  • Atatürk Üniversitesi Adresli: Evet

Özet

Purpose: Reactive oxygen species (ROS), interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) 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-1 beta and TNF-alpha. 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-1 beta and TNF-alpha with acrylamide and the decrease of total glutathione (tGSH) and glutathione reductase (GSHRd) levels in brain tissue. Conclusions: HRE may be useful in the treatment of acrylamide-induced neurotoxicity.