A TNF-? inhibitor abolishes sepsis-induced cognitive impairment in mice by modulating acetylcholine and nitric oxide homeostasis, BDNF release, and neuroinflammation
| dc.contributor.author | Öz, Mehmet | |
| dc.contributor.author | Erdal, Hüseyin | |
| dc.date.accessioned | 2024-07-03T05:59:53Z | |
| dc.date.available | 2024-07-03T05:59:53Z | |
| dc.date.issued | 2024 | |
| dc.department | Tıp Fakültesi | |
| dc.description.abstract | Neurodegenerative disorders have a pathophysiology that heavily involves neuroinflammation. In this study, we used lipopolysaccharide (LPS) to create a model of cognitive impairment by inducing systemic and neuroinflammation in experimental animals. LPS was injected intraperitoneally at a dose of 0.5 mg/kg during the last seven days of the study. Adalimumab (ADA), a TNF-? inhibitor, was injected at a dose of 10 mg/kg a total of 3 times throughout the study. On the last two days of the experiment, 50 mg/kg of curcumin was administered orally as a positive control group. Open field (OF) and elevated plus maze tests (EPM) were used to measure anxiety-like behaviors. The tail suspension test (TST) was used to measure depression-like behaviors, while the novel object recognition test (NOR) was used to measure learning and memory activities. Blood and hippocampal TNF ? and nitric oxide (NO) levels, hippocampal BDNF, CREB, and ACh levels, and AChE activity were measured by ELISA. LPS increased anxiety and depression-like behaviors while decreasing the activity of the learning-memory system. LPS exerted this effect by causing systemic and neuroinflammation, cholinergic dysfunction, and impaired BDNF release. ADA controlled LPS-induced behavioral changes and improved biochemical markers. ADA prevented cognitive impairment induced by LPS by inhibiting inflammation and regulating the release of BDNF and the cholinergic pathway. | |
| dc.identifier.doi | 10.1016/j.bbr.2024.114995 | |
| dc.identifier.issn | 0166-4328 | |
| dc.identifier.scopusquality | Q2 | |
| dc.identifier.uri | https:/dx.doi.org/10.1016/j.bbr.2024.114995 | |
| dc.identifier.uri | https://hdl.handle.net/20.500.12451/12024 | |
| dc.identifier.volume | 466 | en_US |
| dc.identifier.wosquality | N/A | |
| dc.indekslendigikaynak | Web of Science | |
| dc.indekslendigikaynak | Scopus | |
| dc.indekslendigikaynak | PubMed | |
| dc.language.iso | en | |
| dc.publisher | Elsevier B.V. | |
| dc.relation.ispartof | Behavioural Brain Research | |
| dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | |
| dc.rights | info:eu-repo/semantics/embargoedAccess | |
| dc.subject | Adalimumab | |
| dc.subject | Anxiety and Depression | |
| dc.subject | Learning and Memory | |
| dc.subject | Lipopolysaccharide | |
| dc.subject | Neuroinflammation | |
| dc.title | A TNF-? inhibitor abolishes sepsis-induced cognitive impairment in mice by modulating acetylcholine and nitric oxide homeostasis, BDNF release, and neuroinflammation | |
| dc.type | Article |
