| Autor: |
Tanoğlu C; Department of Neurology, Faculty of Medicine, Erzincan Binali Yıldırım University, Erzincan, Turkey; ceydatanoglu@gmail.com., Ersoy A; Department of Neurology, Faculty of Medicine, Erzincan Binali Yıldırım University, Erzincan, Turkey., Çoban TA; Department of Medical Biochemistry, Faculty of Medicine, Erzincan Binali Yıldırım University, Erzincan, Turkey., Yazıcı GN; Department of Histology and Embryology, Erzincan Binali Yıldırım University, Erzincan, Turkey., Mammadov R; Department of Pharmacology, Erzincan Binali Yıldırım University, Erzincan, Turkey., Süleyman B; Department of Pharmacology, Erzincan Binali Yıldırım University, Erzincan, Turkey. |
| Abstrakt: |
Cobalt is a trace element that increases lipid peroxidation and malondialdehyde levels and reduces the antioxidant defense mechanisms of nerve cells. High levels of cobalt exposure may cause peripheral neuropathy, but the mechanism behind this has not yet been elucidated. Taxifolin is a flavonoid whose antioxidant and anti‑inflammatory properties are well‑known. We aimed to investigate the effect of taxifolin on cobalt‑induced oxidative sciatic nerve damage. Eighteen albino male Wistar rats were assigned to three groups: Control, Cobalt, and Taxifolin + Cobalt groups. Total oxidant and total antioxidant status and levels of malondialdehyde, total glutathione, and superoxide dismutase were measured to determine the effect of taxifolin on cobalt‑induced sciatic nerve injury. The following statistically significant effect of taxifolin was observed: It prevented cobalt‑induced oxidative sciatic nerve damage by reducing malondialdehyde levels and total oxidant status and increasing total antioxidant status, total glutathione levels, and superoxide dismutase levels. In a histopathological analysis, we observed similar findings in Control and Taxifolin + Cobalt groups. We determined that taxifolin is effective in preventing cobalt‑induced oxidative damage in sciatic nerve injury. |
