İsmail Gülşen1, Hakan Ak2, Neşe Çölçimen3, Hamit H Alp4, Mehmet E Akyol1, İsmail Demir5, Tugay Atalay6, Ragıp Balahroğlu4, Murat Ç Rağbetli3. 1. Department of Neurosurgery, Yüzüncü Yıl University, School of Medicine, Van, Turkey. 2. Department of Neurosurgery, Bozok University, School of Medicine, Yozgat, Turkey. Electronic address: nrsdrhakanak@yahoo.com. 3. Department of Histology and Embryology, Yüzüncü Yıl University, School of Medicine, Yozgat, Turkey. 4. Department of Biochemistry, Yüzüncü Yıl University, School of Medicine, Yozgat, Turkey. 5. Department of Neurosurgery, Pamukkale University, School of Medicine, Denizli, Turkey. 6. Department of Neurosurgery, Bozok University, School of Medicine, Yozgat, Turkey.
Abstract
BACKGROUND: Traumatic brain injury is a leading cause of morbidity and mortality worldwide. We evaluated the neuroprotective effects of thymoquinone (TQ) in a rat model of traumatic brain injury by using biochemical and histopathologic methods for the first time. MATERIALS AND METHODS: Twenty-four rats were divided into sham (n = 8), trauma (n = 8), and TQ-treated (n = 8) groups. A moderate degree of head trauma was induced with the use of Feeney's falling weight technique, and TQ (5 mg/kg/day) was administered to the TQ-treated group for 7 days. All animals were killed after cardiac perfusion. Brain tissues were extracted immediately after perfusion without damaging the tissues. Biochemical procedures were performed with the serum, and a histopathologic evaluation was performed on the brain tissues. Biochemical experiments included malondialdehyde (MDA), reduced and oxidized coenzyme Q10 analysis, DNA isolation and hydroylazation, and glutathione peroxidase, and superoxide dismutase analyses. RESULTS: Neuron density in contralateral hippocampal regions (CA1, CA2-3, and CA4) 7 days after the trauma decreased significantly in the trauma and TQ-treated groups, compared with that in the control group. Neuron densities in contralateral hippocampal regions (CA1, CA2-3, and CA4) were greater in the TQ-treated group than in the trauma group. TQ did not increase superoxide dismutase or glutathione peroxidase antioxidant levels. However, TQ decreased the MDA levels. CONCLUSIONS: These results indicate that TQ has a healing effect on neural cells after head injury and this effect is mediated by decreasing MDA levels in the nuclei and mitochondrial membrane of neurons.
BACKGROUND:Traumatic brain injury is a leading cause of morbidity and mortality worldwide. We evaluated the neuroprotective effects of thymoquinone (TQ) in a rat model of traumatic brain injury by using biochemical and histopathologic methods for the first time. MATERIALS AND METHODS: Twenty-four rats were divided into sham (n = 8), trauma (n = 8), and TQ-treated (n = 8) groups. A moderate degree of head trauma was induced with the use of Feeney's falling weight technique, and TQ (5 mg/kg/day) was administered to the TQ-treated group for 7 days. All animals were killed after cardiac perfusion. Brain tissues were extracted immediately after perfusion without damaging the tissues. Biochemical procedures were performed with the serum, and a histopathologic evaluation was performed on the brain tissues. Biochemical experiments included malondialdehyde (MDA), reduced and oxidized coenzyme Q10 analysis, DNA isolation and hydroylazation, and glutathione peroxidase, and superoxide dismutase analyses. RESULTS: Neuron density in contralateral hippocampal regions (CA1, CA2-3, and CA4) 7 days after the trauma decreased significantly in the trauma and TQ-treated groups, compared with that in the control group. Neuron densities in contralateral hippocampal regions (CA1, CA2-3, and CA4) were greater in the TQ-treated group than in the trauma group. TQ did not increase superoxide dismutase or glutathione peroxidase antioxidant levels. However, TQ decreased the MDA levels. CONCLUSIONS: These results indicate that TQ has a healing effect on neural cells after head injury and this effect is mediated by decreasing MDA levels in the nuclei and mitochondrial membrane of neurons.
Authors: Heba M Fahmy; Eman R Mohamed; Aida A Hussein; Yasser A Khadrawy; Nawal A Ahmed Journal: BMC Pharmacol Toxicol Date: 2022-06-15 Impact factor: 2.605
Authors: Heba M Fahmy; Mostafa M Ahmed; Ayman S Mohamed; Engy Shams-Eldin; Taiseer M Abd El-Daim; Amena S El-Feky; Amira B Mustafa; Mai W Abd Alrahman; Faten F Mohammed; Mohamed M Fathy Journal: BMC Pharmacol Toxicol Date: 2022-09-26 Impact factor: 2.605