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一氧化氮合酶抑制剂氨基胍增强了亚氨基二丙腈对大鼠的神经毒性。

Nitric oxide synthase inhibitor aminoguanidine potentiates iminodipropionitrile-induced neurotoxicity in rats.

作者信息

Tariq M, Khan H A, Al Deeb S, Al Moutaery K

机构信息

Neuroscience Research Group, Armed Forces Hospital, Riyadh, Saudi Arabia.

出版信息

Neurosci Lett. 1999 Nov 26;276(1):49-52. doi: 10.1016/s0304-3940(99)00789-2.

Abstract

This investigation was undertaken to study the effect of nitric oxide synthase inhibitor, aminoguanidine on iminodipropionitrile (IDPN)-induced neurobehavioral and vestibular toxicity in rats. The dyskinetic syndrome was produced in male Wistar rats by i.p. injections of IDPN (100 mg/kg) for 6 days. Aminoguanidine was administered orally in the doses of 50, 150 and 300 mg/kg, 60 min before IDPN in three different groups. Control rats received vehicle only, whereas another group was treated with 300 mg/kg of aminoguanidine alone (without IDPN). Our results showed that aminoguanidine significantly and dose dependently exacerbated the incidence and intensity of IDPN-induced dyskinetic head movements. Aminoguanidine potentiated IDPN-induced loss of air righting reflex. The histopathological examination of inner ear showed aggravation of IDPN-induced degeneration of sensory hair cells in the crista ampullaris by aminoguanidine. These results suggest the role of nitric oxide in IDPN-induced neurobehavioral and vestibular toxicity.

摘要

本研究旨在探讨一氧化氮合酶抑制剂氨基胍对亚氨基二丙腈(IDPN)诱导的大鼠神经行为和前庭毒性的影响。通过腹腔注射IDPN(100 mg/kg)连续6天,在雄性Wistar大鼠中诱发运动障碍综合征。在三个不同的组中,在注射IDPN前60分钟,分别以50、150和300 mg/kg的剂量口服给予氨基胍。对照大鼠仅接受溶剂,而另一组仅用300 mg/kg的氨基胍治疗(无IDPN)。我们的结果表明,氨基胍显著且剂量依赖性地加剧了IDPN诱导的运动性头部运动的发生率和强度。氨基胍增强了IDPN诱导的翻正反射丧失。内耳的组织病理学检查显示,氨基胍加剧了IDPN诱导的壶腹嵴感觉毛细胞变性。这些结果提示一氧化氮在IDPN诱导的神经行为和前庭毒性中起作用。

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