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Thymoquinone ameliorates amikacin induced oxidative damage in rat brain tissue

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dc.creator ÖZGÖÇMEN, Meltem
dc.creator BİLGİÇ, SEDAT
dc.creator ÖZER, MEHMET KAYA
dc.date 2023-01-01T00:00:00Z
dc.date.accessioned 2023-01-09T12:06:51Z
dc.date.available 2023-01-09T12:06:51Z
dc.identifier b07f1420-3f02-449a-8fc6-3503fcabf075
dc.identifier 10.1080/10520295.2022.2087905
dc.identifier https://avesis.sdu.edu.tr/publication/details/b07f1420-3f02-449a-8fc6-3503fcabf075/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/98255
dc.description We investigated the potential neuroprotective effects of thymoquinone (TQ) on amikacin (AK) induced oxidative damage in rat brain. We used 21 male rats divided randomly into three equal groups. The control group was injected intraperitoneally (i.p.) with 0.5 ml 0.9% aqueous NaCl and given 1 ml 0.9% aqueous NaCl orally. The AK group was administered 1.2 g/kg aqueous AK i.p. as a single dose on the day 3 of the study. The AK + TQ group was given a single 1.2 g/kg dose of AK i.p. on the day 3 of the study plus 40 mg/kg/day TQ by oral gavage daily. Treatment with TQ increased serum ferritin and decreased serum calcium levels significantly. TQ also decreased NADPH oxidase-2, NADPH oxidase-4, and caspase-3 levels. Decreased malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) and catalase (CAT) activities were detected in the AK + TQ group compared to the AK group. TQ administration inhibited lipid peroxide formation and blocked oxidative reactions, which reduced the MDA level and increased SOD and CAT activities induced by AK. Oxidative damage caused by AK was ameliorated by TQ treatment owing to its antioxidative and anti-apoptotic effects. TQ may be a potential therapeutic agent for reducing the severity of AK induced oxidative damage to the brain.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title Thymoquinone ameliorates amikacin induced oxidative damage in rat brain tissue
dc.type info:eu-repo/semantics/article


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