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Scopolamine-Induced Memory Impairment Is Alleviated by Xanthotoxin: Role of Acetylcholinesterase and Oxidative Stress Processes
ACS Chemical Neuroscience ( IF 4.1 ) Pub Date : 2018-01-29 00:00:00 , DOI: 10.1021/acschemneuro.8b00011
Krystyna Skalicka-Wozniak 1 , Barbara Budzynska 2 , Grazyna Biala 2 , Anna Boguszewska-Czubara 3
Affiliation  

Xanthotoxin, popularly occurring furanocoumarin, which can be found in plants from the Apiaceae family, was isolated from fruits of Pastinaca sativa L. by mean of high-performance countercurrent chromatography, and its effects on the scopolamine-induced cognitive deficits in male Swiss mice using the passive avoidance (PA) test were evaluated. To measure the acquisition of memory processes, xanthotoxin (1, 2.5, 5 mg/kg) was administered 30 min before PA test and scopolamine was administered 10 min after xanthotoxin. To measure the consolidation of memory processes, xanthotoxin (1 and 2.5 mg/kg) was injected immediately after removing the mouse from the apparatus and 10 min after scopolamine was administered. In subchronic experiments, mice were injected with xanthotoxin (1 mg/kg) or saline, 6 days, twice daily. At 24 h after the last injection of the drugs, the hippocampus and the prefrontal cortex were removed for biochemical assays. The results demonstrated that either single (2.5 and 5 mg/kg) or repeatable (1 mg/kg) administration of xanthotoxin significantly increased index of latency (IL) in both acquisition and consolidation of memory processes, showing some procognitive effects. The behavioral tests also showed that an acute (2.5 mg/kg) and subchronic (1 mg/kg) administration of xanthotoxin prevent memory impairment induced by injection of scopolamine (1 mg/kg). Observed effects could be due to the inhibition of acetylcholinesterase activities and amelioration of oxidative stress processes in the hippocampus and the prefrontal cortex. It was suggested that xanthotoxin could show neuroprotective effect in scopolamine-induced cognitive impairment connected to cholinergic neurotransmission and oxidative stress in the brain structures.

中文翻译:

花椒毒素减轻了草胺诱导的记忆障碍:乙酰胆碱酯酶和氧化应激过程的作用。

花椒毒素,普遍地存在的呋喃,其可以在从伞形科植物中找到,从果实中分离Pastinaca苜蓿L.通过高效逆流色谱法,使用被动回避(PA)测试评估了它对雄性瑞士小鼠中东pol碱诱导的认知缺陷的影响。为了测量记忆过程的获得,在PA试验前30分钟给予黄嘌呤毒素(1、2.5、5 mg / kg),在黄嘌呤毒素后10分钟给予东pol碱。为了测量记忆过程的巩固,在将小鼠从装置中移出后和东碱施用10分钟后立即注射黄嘌呤毒素(1和2.5 mg / kg)。在亚慢性实验中,每天两次,每天两次给小鼠注射花椒毒素(1 mg / kg)或生理盐水。最后一次注射药物后24小时,将海马和前额叶皮层取出进行生化分析。结果表明,无论是单身(2。黄原毒素的5和5 mg / kg或可重复(1 mg / kg)的给药显着增加了记忆过程的获取和巩固过程中的潜伏期指数(IL),显示出一些认知作用。行为测试还表明,黄嘌呤毒素的急性(2.5 mg / kg)和亚慢性(1 mg / kg)给药可预防东碱(1 mg / kg)注射引起的记忆障碍。观察到的影响可能是由于抑制了海马和前额叶皮层中乙酰胆碱酯酶的活性和氧化应激过程的改善。提示黄嘌呤毒素可以在东pol碱所致的认知障碍中显示神经保护作用,这种认知障碍与胆碱能神经传递和脑结构中的氧化应激有关。
更新日期:2018-01-29
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