The effect of Hippophae rhamnoides L. extract on acrylamideinduced brain injury in rats.
| Autor: | Turan MI; MD, Assistant Professor. Department of Pediatric Neurology - Faculty of Medicine - Gaziantep University - Gaziantep, Turkey., Aktaş M; PhD, Assistant Professor. Department of Biochemistry - Faculty of Medicine - Erzincan Binali Yildirim University - Erzincan, Turkey., Gundogdu B; PhD, Assistant Professor. Department of Pathology - Faculty of Medicine - Ataturk University - Erzurum, Turkey., Yilmaz SK; PhD, Assistant Professor. Nutrition and Dietetics - Erzincan Binali Yildirim University - Erzincan, Turkey., Suleyman H; PhD, Professor. Department of Pharmacology - Faculty of Medicine - Erzincan Binali Yildirim University - Erzincan, Turkey. |
|---|---|
| Jazyk: | angličtina |
| Zdroj: | Acta cirurgica brasileira [Acta Cir Bras] 2021 Nov 22; Vol. 36 (10), pp. e361005. Date of Electronic Publication: 2021 Nov 22 (Print Publication: 2021). |
| DOI: | 10.1590/ACB361005 |
| Abstrakt: | 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. Conclusions: HRE may be useful in the treatment of acrylamide-induced neurotoxicity. |
| Databáze: | MEDLINE |
| Externí odkaz: |
|