Zingiberene attenuates hydrogen peroxide-induced toxicity in neuronal cells

被引:11
|
作者
Togar, B. [1 ]
Turkez, H. [2 ]
Stefano, A. D. [3 ]
Tatar, A. [4 ]
Cetin, D. [5 ]
机构
[1] Ataturk Univ, Dept Biol, Fac Sci, TR-25240 Erzurum, Turkey
[2] Erzurum Tech Univ, Dept Mol Biol & Genet, Fac Sci, Erzurum, Turkey
[3] Univ G DAnnunzio, Dept Pharmacol, Chieti, Italy
[4] Ataturk Univ, Dept Med Genet, Fac Med, TR-25240 Erzurum, Turkey
[5] Ataturk Univ, Dept Med Pharmacol, Fac Med, TR-25240 Erzurum, Turkey
关键词
Zingiberene; neuroprotective action; H2O2; cultured neuron; DNA damage; oxidative stress; OXIDATIVE STRESS; DNA-DAMAGE; IN-VITRO; H2O2-INDUCED APOPTOSIS; CHEMICAL-COMPOSITION; PC12; CELLS; BORIC-ACID; GENOTOXICITY; NEUROTOXICITY; SURVIVAL;
D O I
10.1177/0960327114538987
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
In this experimental design, we explored the neuroprotective potential of zingiberene (ZGB), a monocyclic sesquiterpene, in hydrogen peroxide (H2O2)-induced toxicity in newborn rat cerebral cortex cell cultures for the first time. The rats were exposed to H2O2 for 6 h to determine the oxidative stress levels. To evaluate cell viability, both 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assays were carried out. Total antioxidant capacity (TAC) and total oxidative stress (TOS) parameters were used to evaluate oxidative changes. Besides determining 8-hydroxy-2-deoxyguanosine (8-OH-dG) levels in vitro, single-cell gel electrophoresis was also performed to measure the resistance of neuronal DNA to H2O2- exposed rats. Our results showed that survival and TAC levels of the cells decreased, while TOS, 8-OH-dG levels and the mean values of the total scores of cells showing DNA damage increased in the H2O2 alone-treated cultures. But pretreatment of ZGB suppressed the cytotoxicity, genotoxicity and oxidative stress that were increased by H2O2. Based on these observations, it is suggested that the sesquiterpene ZGB can be used as a novel and natural potential therapeutic in counteracting oxidative damages in the field of neurodegenerative disorders.
引用
收藏
页码:135 / 144
页数:10
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