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dc.contributor.authorÇelik, H. and Kandemir, F.M. and Caglayan, C. and Özdemir, S. and Çomaklı, S. and Kucukler, S. and Yardım, A.
dc.date.accessioned2021-04-08T12:06:26Z
dc.date.available2021-04-08T12:06:26Z
dc.date.issued2020
dc.identifier10.1007/s11033-020-05302-z
dc.identifier.issn03014851
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85078971764&doi=10.1007%2fs11033-020-05302-z&partnerID=40&md5=f6015aae48d46d9a562256679a03b36f
dc.identifier.urihttp://acikerisim.bingol.edu.tr/handle/20.500.12898/3930
dc.description.abstractThe purpose of the current study was to examine the neuroprotective effect of rutin against colistin-induced neurotoxicity in rats. Thirty-five male Sprague Dawley rats were randomly divided into 5 groups. The control group (orally received physiological saline), the rutin group (orally administered 100 mg/kg body weight), the colistin group (i.p. administered 15 mg/kg body weight), the Col + Rut 50 group (i.p. administered 15 mg/kg body weight of colistin, and orally received 50 mg/kg body weight of rutin), the Col + Rut 100 group (i.p. administered 15 mg/kg body weight of colistin, and orally received 100 mg/kg body weight of rutin). Administration of colistin increased levels of glial fibrillary acidic protein and brain-derived neurotrophic factor and acetylcholinesterase and butyrylcholinesterase activities while decreasing level of cyclic AMP response element binding protein and extracellular signal regulated kinases 1 and 2 (ERK1/2) expressions. Colistin increased oxidative impairments as evidenced by a decrease in level of nuclear factor erythroid 2-related factor 2 (Nrf-2), glutathione, superoxide dismutase, glutathione peroxidase and catalase activities, and increased malondialdehyde content. Colistin also increased the levels of the apoptotic and inflammatoric parameters such as cysteine aspartate specific protease-3 (caspase-3), p53, B-cell lymphoma-2 (Bcl-2), nuclear factor kappa B (NF-κB), Bcl-2 associated X protein (Bax), tumor necrosis factor-α (TNF-α) and neuronal nitric oxide synthase (nNOS). Rutin treatment restored the brain function by attenuating colistin-induced oxidative stress, apoptosis, inflammation, histopathological and immunohistochemical alteration suggesting that rutin supplementation mitigated colistin-induced neurotoxicity in male rats. © 2020, Springer Nature B.V.
dc.language.isoEnglish
dc.sourceMolecular Biology Reports
dc.titleNeuroprotective effect of rutin against colistin-induced oxidative stress, inflammation and apoptosis in rat brain associated with the CREB/BDNF expressions


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