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首页> 外文期刊>Experimental Neurology >Protection by 2-deoxy-D-glucose against beta,beta'-iminodipropionitrile-induced neurobehavioral toxicity in mice.
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Protection by 2-deoxy-D-glucose against beta,beta'-iminodipropionitrile-induced neurobehavioral toxicity in mice.

机译:2-脱氧-D-葡萄糖对小鼠中β,β'-亚氨基二丙腈的神经行为毒性的保护作用。

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This investigation was undertaken to study the effect of 2-deoxy-D-glucose (2-DG) on beta, beta'-iminodipropionitrile (IDPN)-induced neurobehavioral toxicity in mice. Animals were divided into five groups of nine animals each. One of the groups served as control and received vehicle only, whereas the remaining four groups were treated with IDPN (250 mg/kg, i.p.) daily for 11 days. 2-DG was injected intraperitoneally in the doses of 0 (vehicle only), 100, 300, and 600 mg/kg daily 30 min before IDPN administration. The animals were observed for dyskinetic behavior including vertical (retrocollis) and horizontal (laterocollis) head movements and circling. Twenty-four hours after the last dose of IDPN, the animals were sacrificed by decapitation and striata were isolated from the brain for the analysis of serotonin (5-HT). Our results showed that 2-DG significantly and dose dependently attenuated the incidence and severity of IDPN-induced neurobehavioral toxicity. Administration of 2-DG also protected mice against IDPN-induced increase in striatal 5-HT levels. Further studies are warranted to investigate the neuroprotective mechanism of 2-DG against IDPN-induced neurotoxicity.
机译:进行该研究以研究2-脱氧-D-葡萄糖(2-DG)对β,β'-亚氨基二丙腈(IDPN)诱导的小鼠神经行为毒性的影响。将动物分为五组,每组九只动物。一组用作对照并仅接受媒介物,而其余四组每天接受IDPN(250 mg / kg,腹腔注射)治疗11天。在IDPN给药前30分钟,每天以0(仅用于车辆),100、300和600 mg / kg的剂量腹膜内注射2-DG。观察到动物的运动障碍行为,包括垂直(逆行结肠)和水平(腹泻)头部运动和盘旋。在最后一次注射IDPN后24小时,将动物断头处死,并从大脑中分离出纹状体,以分析5-羟色胺(5-HT)。我们的结果表明,2-DG显着且剂量依赖性地减弱了IDPN诱导的神经行为毒性的发生率和严重性。施用2-DG还可以保护小鼠免受IDPN诱导的纹状体5-HT水平升高。有必要进行进一步的研究以研究2-DG对IDPN诱导的神经毒性的神经保护机制。

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