Toxic Effects of Isoniazid and Rifampicin on Rat Brain Tissue: The Preventive Role of Caffeic Acid Phenethyl Ester

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dc.contributor.authorCevik, Mehmet Ugur
dc.contributor.authorAcar, Abdullah
dc.contributor.authorTanriverdi, Halis
dc.contributor.authorVarol, Sefer
dc.contributor.authorArikanoglu, Adalet
dc.contributor.authorYucel, Yavuz
dc.contributor.authorAkil, Esref
dc.date.accessioned2024-04-24T17:21:13Z
dc.date.available2024-04-24T17:21:13Z
dc.date.issued2012
dc.departmentDicle Üniversitesien_US
dc.description.abstractTo the best of present knowledge, the possible protective effects of Caffeic Acid Phenethyl Ester (CAPE), on possible Isoniazid (INH) and Rifampicin (RIF) induced neurotoxic effects in brain tissue have not been investigated yet. As such, the purpose of this experimental study was to investigate the effects of CAPE, on INH and RIF induced neurotoxicity in rat brain tissue. We measured Total Antioxidant Capacity (TAC), Superoxide Dismutase (SOD) activities, Malondialdehyde (MDA) and nitric oxide (NO) levels in the brain tissue of rats. Male Sprague-Dawley rats were divided into eight experimental groups, with ten animals in each group. These groups are consist of control group, INH-treated group, RIF-treated group, INH+RIF treated group, INH+CAPE treated group, RIF+CAPE treated group, INH+RIF+CAPE treated group and CAPE treated group. MDA and SOD levels in brain tissue were significantly higher and TAC levels were lower in the INH, RIF and INH+RIF treated groups (p<0.05) and TAC levels were lower in the INH, RIF and INH+RIF groups than in the control group (p<0.05). CAPE plus INH and/or RIF treatment caused a significant decrease in MDA levels in brain tissue (p<0.05). In addition, CAPE plus INH and/or RIF treatment caused a significant increase in TAC levels (p<0.05). In conclusion, we have shown that administration of INH and RIF is accompanied by increased lipid peroxidation and oxidants in rat brain tissue. CAPE may protect against INH and RIF-induced neurotoxicity. Therefore, CAPE supplementation may be used as a potential neuroprotective drug for antituberculosis therapy with INH and/or RIF.en_US
dc.identifier.doi10.3923/ijp.2012.555.560
dc.identifier.endpage560en_US
dc.identifier.issn1811-7775
dc.identifier.issn1812-5700
dc.identifier.issue6en_US
dc.identifier.scopus2-s2.0-84866063244
dc.identifier.scopusqualityN/A
dc.identifier.startpage555en_US
dc.identifier.urihttps://doi.org/10.3923/ijp.2012.555.560
dc.identifier.urihttps://hdl.handle.net/11468/19410
dc.identifier.volume8en_US
dc.identifier.wosWOS:000316977400014
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoenen_US
dc.publisherAsian Network Scientific Information-Ansineten_US
dc.relation.ispartofInternational Journal of Pharmacology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectIsoniaziden_US
dc.subjectRifampicinen_US
dc.subjectOxidative Stressen_US
dc.subjectCaffeic Acid Phenethyl Esteren_US
dc.subjectNeurotoxicityen_US
dc.titleToxic Effects of Isoniazid and Rifampicin on Rat Brain Tissue: The Preventive Role of Caffeic Acid Phenethyl Esteren_US
dc.titleToxic Effects of Isoniazid and Rifampicin on Rat Brain Tissue: The Preventive Role of Caffeic Acid Phenethyl Ester
dc.typeArticleen_US

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