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首页> 外文期刊>Archives of pharmacal research >Protective effects of acetyl-L-carnitine on neurodegenarative changes in chronic cerebral ischemia models and learning-memory impairment in aged rats
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Protective effects of acetyl-L-carnitine on neurodegenarative changes in chronic cerebral ischemia models and learning-memory impairment in aged rats

机译:乙酰左旋肉碱对老年大鼠慢性脑缺血模型神经退行性变化和学习记忆障碍的保护作用

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This study investigated the effects of acetyl-L-carnitine (ALC) in secondarily-induced cerebral chronic ischemia models using rats with permanent ligation of bilateral common carotid arteries (BCCL) and spontaneously hypertensive rats (SHR). Additionally, we used normal aged rats as a primary dementia model. Chronic ALC administration at 100 mg/kg (p.o.) for 4 weeks significantly attenuated neurodegenerative changes. In groups receiving 50 mg/kg or 100 mg/kg, ALC inhibited the active astrocyte increase in cerebral tissues of both BCCL and SHR models. In BCCL rats, ALC administration (50 mg/kg or 100 mg/kg, p.o.) resulted in significant promotion of glutathione levels in brain tissues. We also confirmed behavioral improvement after ALC treatment (100 mg/kg for 8 weeks, p.o.) on learning-memory function using aged rats (18 months old) in a passive avoidance task and preservation of CA1 pyramidal neurons was coincided on histopathological observation. In conclusion, chronic ALC administration may ameliorate cerebral ischemia progress after a cerebrovascular disorder as well as spontaneous ageing-related cerebral dysfunction via hippocampal protection.
机译:这项研究调查了永久性结扎双侧颈总动脉(BCCL)的大鼠和自发性高血压大鼠(SHR)在继发性脑慢性缺血模型中乙酰-L-肉碱(ALC)的作用。此外,我们使用正常的老年大鼠作为原发性痴呆模型。以100 mg / kg(p.o.)进行4周的慢性ALC给药可显着减轻神经退行性变化。在接受50 mg / kg或100 mg / kg的组中,ALC抑制了BCCL和SHR模型的大脑组织中活性星形胶质细胞的增加。在BCCL大鼠中,ALC(50 mg / kg或100 mg / kg,p.o。)给药可显着促进脑组织中谷胱甘肽水平的升高。我们还证实了ALC治疗(100 mg / kg持续8周,p.o.)在使用成年大鼠(18个月大)进行被动回避任务中的学习记忆功能方面的行为改善,并且在组织病理学观察中同时保留了CA1锥体神经元。总之,通过海马保护,长期给予ALC可以改善脑血管疾病以及与衰老相关的自发性脑功能障碍后的脑缺血进程。

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