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首页> 外文期刊>BMB Reports >Neuroprotective effects of the antioxidant action of 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride against ischemic neuronal damage in the brain
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Neuroprotective effects of the antioxidant action of 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride against ischemic neuronal damage in the brain

机译:2-环丙基氨基-3-甲基-1,3-噻唑盐酸盐抗氧化作用对大脑缺血性神经元损伤的神经保护作用

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Ischemia is characterized by oxidative stress and changes in the antioxidant defense system. Our recent in vitro study showed that 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride protects cortical astrocytes against oxidative stress. In the current study, we examined the effects of 2-cyclopropylimino-3-methyl- 1,3-thiazoline hydrochloride on ischemia-induced neuronal damage in a gerbil ischemia/reperfusion models. Extensive neuronal death in the hippocampal CA1 area was observed 4 days after ischemia/reperfusion. Intraperitoneal injection of 2-cyclopropylimino- 3-methyl-1,3-thiazoline hydrochloride (0.3 mg/kg body weight) significantly prevented neuronal death in the CA1 region of the hippocampus in response to transient forebrain ischemia. 2-Cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride administration reduced ischemia-induced increases in reactive oxygen species levels and malondialdehyde content. It also attenuated the associated reductions in glutathione level and superoxide dismutase, catalase, and glutathione peroxidase activities. Taken together, our results suggest that 2-cyclopropylimino- 3-methyl-1,3-thiazoline hydrochloride protects against ischemia-induced neuronal damage by reducing oxidative stress through its antioxidant actions.
机译:缺血的特征在于氧化应激和抗氧化防御系统的变化。我们最近的体外研究表明,2-环丙基氨基-3-甲基-1,3-噻唑啉盐酸盐保护皮质星形胶质细胞免受氧化应激。在目前的研究中,我们研究了2-环丙基氨基-3-甲基-1,3-噻唑啉盐酸盐对Gerbil缺血/再灌注模型中缺血诱导的神经元损伤的影响。在缺血/再灌注后4天观察海马CA1区域的广泛神经元死亡。腹膜内注射2-环丙基氨基-3-甲基-1,3-噻唑啉盐酸盐(0.3mg / kg体重)显着防止了海马CA1区的神经元死亡,响应于瞬态前脑缺血。 2-环丙基氨基-3-甲基-1,3-噻唑啉盐酸盐施用降低了活性氧物质水平和丙二醛含量的缺血诱导的增加。它还减弱了谷胱甘肽水平和超氧化物歧化酶,过氧化氢酶和谷胱甘肽过氧化物酶活性的相关减少。我们的结果表明,通过通过其抗氧化作用降低氧化胁迫,将2-环丙基氨基-3-甲基-1,3-噻唑啉盐酸盐免受氧化胁迫来保护缺血诱导的神经元损伤。

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