dc.contributor.author | Solmaz, V. | |
dc.contributor.author | Kaya, M. | |
dc.contributor.author | Uslu, F.B. | |
dc.contributor.author | Atasoy, O. | |
dc.contributor.author | Erbaş, O. | |
dc.date.accessioned | 2022-11-04T19:55:45Z | |
dc.date.available | 2022-11-04T19:55:45Z | |
dc.date.issued | 2022 | |
dc.identifier.issn | 0894-1939 | |
dc.identifier.uri | https://doi.org/10.1080/08941939.2020.1809751 | |
dc.identifier.uri | http://hdl.handle.net/11446/4618 | |
dc.description.abstract | Aim: Our aim was to investigate the possible neuroprotective properties of papaverine in sepsis-induced critical illness neuropathy (SCIN) through the evaluation of various inflammatory biochemical markers, including interleukin 6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-α), and oxidative stress biomarkers, such as malondialdehyde (MDA) and lactic acid. Additionally, evaluation of the HMGB1/RAGE interactions in SCIN was another target of this research. Method: To create a sepsis model, a procedure involving intraperitoneal injection of feces was performed on 48 rats. The rats were divided into four equal groups: sham operated, controls and those receiving 20 and 40 mg/kg/day papaverine. After five-day treatments, compound muscle action potential (CMAPs) with electroneuromyography (ENMG) was recorded in all rats. Following ENMG evaluations, the plasma levels of sRAGE, HMGB1, TNF-α, IL-6, CRP, MDA and lactic acid were measured. Results: TNF-α, CRP, IL-6, HMGB1, MDA, and lactic acid levels were significantly elevated in the SCIN group, and sRAGE levels were significantly decreased. In recipients of papaverine (20 and 40 mg/kg) treatment, these biochemical findings were improved. Furthermore, electrophysiological findings also showed significant improvement in both 20 and 40 mg/kg papaverine treated groups. Conclusion: Papaverine demonstrates neuroprotective effects in a rat model of SCIN. Considering its anti-inflammatory and antioxidant properties, papaverine’s neuroprotective effects possibly stem from the suppression of the RAGE-HMGB1 axis. (Figure presented.). © 2020 Taylor & Francis Group, LLC. | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Taylor and Francis Ltd. | en_US |
dc.relation.ispartof | Journal of Investigative Surgery | en_US |
dc.identifier.doi | 10.1080/08941939.2020.1809751 | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | and lactic acid | en_US |
dc.subject | CMAP | en_US |
dc.subject | Critical illness polyneuropathy | en_US |
dc.subject | CRP | en_US |
dc.subject | HMGB1 | en_US |
dc.subject | IL-6 | en_US |
dc.subject | MDA | en_US |
dc.subject | papaverine | en_US |
dc.subject | sRAGE | en_US |
dc.subject | TNF-α | en_US |
dc.subject | advanced glycation end product receptor | en_US |
dc.subject | C reactive protein | en_US |
dc.subject | high mobility group B1 protein | en_US |
dc.subject | interleukin 6 | en_US |
dc.subject | ketamine | en_US |
dc.subject | lactic acid | en_US |
dc.subject | malonaldehyde | en_US |
dc.subject | papaverine | en_US |
dc.subject | thiobarbituric acid reactive substance | en_US |
dc.subject | tumor necrosis factor | en_US |
dc.subject | xylazine | en_US |
dc.subject | adult | en_US |
dc.subject | animal experiment | en_US |
dc.subject | animal model | en_US |
dc.subject | animal tissue | en_US |
dc.subject | antioxidant activity | en_US |
dc.subject | Article | en_US |
dc.subject | controlled study | en_US |
dc.subject | electroneuromyography | en_US |
dc.subject | electrophysiology | en_US |
dc.subject | enzyme linked immunosorbent assay | en_US |
dc.subject | feces | en_US |
dc.subject | lipid peroxidation | en_US |
dc.subject | male | en_US |
dc.subject | muscle action potential | en_US |
dc.subject | neuropathy | en_US |
dc.subject | neuroprotection | en_US |
dc.subject | nonhuman | en_US |
dc.subject | oxidative stress | en_US |
dc.subject | protein blood level | en_US |
dc.subject | rat | en_US |
dc.subject | sepsis | en_US |
dc.subject | temperature | en_US |
dc.title | Papaverine Has Therapeutic Potential for Sepsis-Induced Neuropathy in Rats, Possibly via the Modulation of HMGB1-RAGE Axis and Its Antioxidant Prosperities | en_US |
dc.type | article | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.volume | 35 | en_US |
dc.identifier.startpage | 7 | en_US |
dc.identifier.endpage | 13 | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.department-temp | Solmaz, V., Department of Neurology, Memorial Hizmet Hospital, Istanbul, Turkey; Kaya, M., Department of Internal Medicine, Memorial Hizmet Hospital, Istanbul, Turkey; Uslu, F.B., Department of Anesthesiology, Batman State Hospital, Batman, Turkey; Atasoy, O., Radiation Oncology, Kartal Dr. Lutfi Kırdar Traning and Research Hospital, Istanbul, Turkey; Erbaş, O., Medical Faculty, Department of Physiology, Demiroğlu Bilim University, Istanbul, Turkey | en_US |
dc.identifier.pmid | 32842806 | en_US |
dc.identifier.scopus | 2-s2.0-85089863009 | en_US |
dc.authorscopusid | 55357225500 | |
dc.authorscopusid | 57542543400 | |
dc.authorscopusid | 57076695100 | |
dc.authorscopusid | 57216297567 | |
dc.authorscopusid | 55469991100 | |