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Effect of melatonin co-treatment against kainic acid on thiol redox modulator gene expressions in rat Hippocampus
Guliz Armagan, Ezgi Turunc Bayrakdar, Lutfiye Kanıt and Ayfer Yalcin
Kainic acid (KA)-induced neurotoxicity is mediated by oxidative stress, and melatonin (Mel), an antioxidant pineal hormone, provides neuroprotection against KA. The maintenance of intracellular redox homeostasis in brain is essential for neuronal survival and the regulation of redox homeostasis is provided by thiol containing molecules such as glutathione (GSH), thioredoxin (Trx)/thioredoxin reductase (TrxR) and redox factor-1 (Ref-1). In this study, we aimed to determine the effect of melatonin treatment on gene expressions of Trx, TrxR and Ref-1 against KA in rat hippocampus. Our results show that the levels of TrxR mRNA significantly increased in Mel+KA when compared to controls (p<0.01) and Mel only (p<0.05). The Mel only treatment significantly decreased the expression of Ref-1 mRNA. Also, there was a significant difference in the expression of Ref-1 mRNA between Mel+KA and Mel only (p<0.01). However, there was no significant change in the expressional levels of Trx mRNA in Mel- and Mel+KA-treated rats. Our results may suggest that melatonin plays a role in the regulation of thiol redox modulator genes in the brain in order to maintain cellular redox homeostasis against KA-induced oxidative stress.
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Effect of melatonin co-treatment against kainic acid on thiol redox modulator gene expressions in rat Hippocampus
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