| Makale Türü |
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| Dergi Adı | Journal of Cellular Neuroscience and Oxidative Stress | ||
| Dergi ISSN | 2149-7222 Scopus Dergi | ||
| Dergi Tarandığı Indeksler | Scopus | ||
| Makale Dili | İngilizce | Basım Tarihi | 09-2023 |
| Cilt / Sayı / Sayfa | 15 / 2 / 1147–1156 | DOI | 10.37212/jcnos.1365512 |
| Makale Linki | https://dergipark.org.tr/tr/pub/jcnos/issue/80146/1365512 | ||
| Özet |
Thirty-six C57BL/6j black mice were divided into the control groups of ACA, GTN, and ACA+GTN. Mice in the ACA were treated intraperitoneally with ACA (25 mg/kg) for three days. Mice in the GTN were treated intraperitoneally with a single dose of GTN (10 mg/kg) for migraine induction. After the experimental stages were completed, the mice in all groups were sacrificed, and brain tissue and erythrocyte samples were taken from the mice. The levels of inflammatory cytokines (TNF α, IL 1β, and IL 6), apoptosis, intracellular ROS, lipid peroxidation, caspase 3-9, and mitochondrial membrane potential increased in the GTN group. However, their levels were decreased in the ACA+GTN group by the injection of ACA. The treatment of ACA regulated the GTN treatment-induced decreases of glutathione levels, glutathione peroxidase activation, and cell viability in the brain and erythrocytes. In conclusion, GTN plays a role in neurotoxicity caused by increased apoptosis and ROS. We observed that ACA modulated the brain and erythrocyte oxidant, antioxidant parameters, and apoptotic processes. The neuro-protective role of ACA treatment may be explained by its modulating activity against increased apoptosis and oxidative stress. |
| Anahtar Kelimeler |
| Apoptosis | Brain | Experimental migraine | Glutathione | Inflammatory cytokines |
| Atıf Sayıları | |
| Scopus | 1 |
| Google Scholar | 3 |
| Dergi Adı | Journal of Cellular Neuroscience and Oxidative Stress |
| Yayıncı | Suleyman Demirel University |
| Açık Erişim | Hayır |
| E-ISSN | 2149-7222 |
| CiteScore | 1,0 |
| SJR | 0,141 |
| SNIP | 0,445 |