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dc.contributor.authorGonullu, Edip
dc.contributor.authorDagistan, Gozde
dc.contributor.authorErkin, Yuksel
dc.contributor.authorErdogan, Mumin Alper
dc.contributor.authorErbas, Oytun
dc.date.accessioned2024-02-04T13:29:53Z
dc.date.available2024-02-04T13:29:53Z
dc.date.issued2023
dc.identifier.issn0006-9248
dc.identifier.issn1336-0345
dc.identifier.urihttps://doi.org/10.4149/BLL_2023_010
dc.identifier.urihttp://hdl.handle.net/11446/4779
dc.description.abstractCisplatin is commonly used in the treatment of lung, genitourinary, and gastrointestinal cancers. Peripheral neuropathy is the most important side effect, leading to a decrease in the dose of cisplatin or its complete cessation in the early period. 16 rats were given cisplatin at a dose of 2.5 mg/ kg/day twice a week for 4 weeks to induce neuropathy model. The rats taking Cisplatin were divided into 2 groups. Group 1 rats (n = 8) were given 1 ml/kg/day 0.9 % NaCl intraperitoneally, and Group 2 rats were given 10 mg/kg/day Propofol intraperitoneally daily for 4 weeks. The remaining 8 rats served as the control group. At the end of the study, all animals were tested for motor functions. Blood samples were collected for the measurement of plasma lipid peroxidation (malondialdehyde; MDA), tumor necrosis factor (TNF-alpha), glutathione (GSH), IL-6 and HSP-70 levels. Electromyography findings revealed that compound muscle action potential (CMAP) amplitude was significantly higher in the cisplatin-Propofol group than in the cisplatin-saline group. Also, cisplatin-Propofol treated group showed significantly lower TNF-alpha, MDA and IL-6 levels and higher GSH and HSP-70 levels than cispalatin-Saline group (p < 0.01, p < 0.001). In addition, while the CMAP latency was decreased in the propofol group, the CMAP amplitude was increased, and a significant improvement was observed in the Inclined test scores. Besides, histological examinations showed an increase in axon diameter and NGF expression with Propofol treatment. This study demonstrated that Propofol exerts protective activity against cisplatin-induced neurotoxicity by increasing endogenous antioxidants and reducing lipid peroxidation and inflammation (Tab. 3, Fig. 4, Ref. 30). Text in PDF www.elis.sken_US
dc.language.isoengen_US
dc.publisherAepress Sroen_US
dc.relation.ispartofBratislava Medical Journal-Bratislavske Lekarske Listyen_US
dc.identifier.doi10.4149/BLL_2023_010
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectcisplatinen_US
dc.subjectneuropathyen_US
dc.subjectpropofolen_US
dc.subjectoxidative damageen_US
dc.subjectinflammationen_US
dc.titleDemonstration of the protective effect of propofol in rat model of cisplatin-induced neuropathyen_US
dc.typearticleen_US
dc.departmentDBÜen_US
dc.identifier.issue1en_US
dc.identifier.volume124en_US
dc.identifier.startpage64en_US
dc.identifier.endpage69en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.department-temp[Gonullu, Edip] Izmir Bakircay Univ, Anesthesiol & Reanimat Dept Algol, Fac Med, Izmir, Turkiye; [Dagistan, Gozde] Akdeniz Univ, Anesthesiol & Reanimat Dept Algol, Fac Med, Antalya, Turkiye; [Erkin, Yuksel] Dokuz Eylul Univ, Anesthesiol & Reanimat Dept Algol, Fac Med, Izmir, Turkiye; [Erdogan, Mumin Alper] Izmir Katip Celebi Univ, Dept Physiol, Fac Med, Izmir, Turkiye; [Erbas, Oytun] Demiroglu Bilim Univ, Dept Physiol, Fac Med, Istanbul, Turkiyeen_US
dc.authoridErbas, Oytun/0000-0001-5427-8428
dc.identifier.pmid36519610en_US
dc.identifier.scopus2-s2.0-85144586065en_US
dc.identifier.wosWOS:001092683600009en_US


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