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首页> 外文期刊>Oriental pharmacy and experimental medicine >Effect of ammonium glycyrrhizinate on haloperidol- and reserpine- induced neurobehavioral alterations in experimental paradigms
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Effect of ammonium glycyrrhizinate on haloperidol- and reserpine- induced neurobehavioral alterations in experimental paradigms

机译:甘草次酸铵对氟哌啶醇和利血平诱导的实验行为神经行为改变的影响

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摘要

The present work was aimed to assess the effect of ammonium glycyrrhizinate, AG (50, 100, and 150?mg/kg, i.p.) on haloperidol induced catalepsy in mice; reserpine induced orofacial dyskinesia in rats; and reserpine antagonism in mice. Additionally the effect of AG on lipid peroxidation (LP) in cataleptic mice brain and monoamine oxidase-B (MAO-B) levels in normal mice brain was assessed. Administration of AG 100 and 150?mg/kg showed significant reduction in the duration of cataleptic behavior at 60 to 180?min and dose dependent decrease in LP induced by haloperidol. AG showed significant decrease in frequency of vacuous chewing movements at 150?mg/kg and frequency of tongue protrusion at 100 and 150?mg/kg in reserpine induced orofacial dyskinesia test. AG showed significant increase in frequency of horizontal movement and rearing behavior at 150?mg/kg and increase in grooming behavior at 100 and 150?mg/kg in reserpine antagonism test. AG showed dose dependent inhibition of MAO-B in the normal mice brain. These results suggested that AG prevented the haloperidol- and reserpine- induced neurobehavioral alterations possibly by acting as free radical scavenger or inhibiting MAO-B thereby increasing dopaminergic transmition consequently decreasing dopamine metabolites and ultimately preventing the generation of free radicals.
机译:目前的工作旨在评估甘草酸铵 AG (50、100和150?mg / kg,i.p。)对氟哌啶醇引起的小鼠僵直症的影响;利血平引起的大鼠口面部运动障碍;和利血平对小鼠的拮抗作用。此外,还评估了 AG 对感性小鼠大脑脂质过氧化(LP)和正常小鼠大脑中单胺氧化酶B(MAO-B)水平的影响。给予100和150?mg / kg的 AG 时,在60至180?min时,致敏行为的持续时间显着减少,而氟哌啶醇诱导的LP剂量依赖性降低。 AG 在利血平诱发的口面运动障碍试验中,空腹咀嚼运动的频率在150?mg / kg时显着降低,舌头突出频率在100和150?mg / kg时显着降低。 AG 在利血平拮抗试验中,水平移动和饲养行为的频率显着增加,分别为150?mg / kg和100和150?mg / kg。 AG 在正常小鼠的大脑中显示出MAO-B的剂量依赖性抑制作用。这些结果表明 AG 可能通过充当自由基清除剂或抑制MAO-B来预防氟哌啶醇和利血平诱导的神经行为改变,从而增加多巴胺能传递,从而减少多巴胺代谢产物并最终预防自由基的产生。

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