Effects of immune cell-targeted treatments result from the suppression of neuronal oxidative stress and inflammation in experimental diabetic rats

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dc.authorid0000-0002-5926-9210en_US
dc.authorid0000-0001-8312-5156en_US
dc.authorid0000-0002-3233-8044en_US
dc.contributor.authorMert, Tufan
dc.contributor.authorŞahin, Emel
dc.contributor.authorYaman, Selma
dc.contributor.authorŞahin, Mehmet
dc.date.accessioned2021-06-23T19:54:15Z
dc.date.available2021-06-23T19:54:15Z
dc.date.issued2020
dc.departmentBAİBÜ, Tıp Fakültesi, Temel Tıp Bilimleri Bölümüen_US
dc.description.abstractIn this study, we hypothesized that reduction of immune cell activation as well as their oxidant or inflammatory mediators with minocycline (MCN), liposome-encapsulated clodronate (LEC), or anti-Ly6G treatments can be neuroprotective approaches in diabetic neuropathy. MCN (40 mg/kg) for reduction of microglial activation, LEC (25 mg/kg) for of macrophage inhibition, or anti-Ly6G (150 mu g/kg) for neutrophil suppression injected to streptozotocin (STZ)-induced diabetic rats twice, 3 days, and 1 week (half dose) after STZ. Animal mass and blood glucose levels were measured; thermal and mechanical sensitivities were tested for in pain sensations. The levels of chemokine C-X-C motif ligand 1 (CXCL1), CXCL8, and C-C motif ligand 2 (CCL2), CCL3, and total oxidant status (TOS) and total antioxidant status (TAS) were measured in the spinal cord and sciatic nerve tissues of rats. LEC significantly reduced the glucose level of diabetic rats compared with drug control. However, MCN or anti-LY6G did not change the glucose level. While diabetic rats showed a marked decrease in both thermal and mechanical sensations, all treatments alleviated these abnormal sensations. The levels of chemokines and oxidative stress parameters increased in diabetic rats. All drug treatments significantly decreased the CCL2, CXCL1, and CXCL8 levels of spinal cord tissues and ameliorated the neuronal oxidative stress compared with control treatments. Present findings suggest that the neuroprotective actions of MCN, LEC, or anti-Ly6G treatments may be due to the modulation of neuronal oxidative stress and/or inflammatory mediators of immune cells in diabetic rats with neuropathy.en_US
dc.identifier.doi10.1007/s00210-020-01871-9
dc.identifier.endpage1302en_US
dc.identifier.issn0028-1298
dc.identifier.issn1432-1912
dc.identifier.issue7en_US
dc.identifier.pmid32361779en_US
dc.identifier.scopus2-s2.0-85085066379en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage1293en_US
dc.identifier.urihttps://doi.org/10.1007/s00210-020-01871-9
dc.identifier.urihttps://hdl.handle.net/20.500.12491/10477
dc.identifier.volume393en_US
dc.identifier.wosWOS:000530261200001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorMert, Tufan
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofNaunyn-Schmiedebergs Archives Of Pharmacologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectDiabetesen_US
dc.subjectNeuronal Chemokinesen_US
dc.subjectNeuronal Oxidative Stressen_US
dc.subjectImmune Cellsen_US
dc.subjectRatsen_US
dc.titleEffects of immune cell-targeted treatments result from the suppression of neuronal oxidative stress and inflammation in experimental diabetic ratsen_US
dc.typeArticleen_US

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