Gupta Gaurav, Chellappan Dinesh K, Agarwal Mohit, Ashwathanarayana Madhu, Nammi Srinivas, Pabreja Kavita, Dua Kamal
School of Medicine and Public Health, University of Newcastle, Newcastle, NSW 2308. Australia.
School of Pharmacy, International Medical University, Kuala Lumpur 57000. Malaysia.
Cent Nerv Syst Agents Med Chem. 2017;17(3):196-200. doi: 10.2174/1871524917666161111095335.
Elevation in brain levels of aluminium can be neurotoxic and can cause learning and memory deficiencies. In Chinese medicine, Morus alba is used as a neuroprotective herb. The current study was intended to discover the recuperative effect of morusin against aluminium trichloride (AlCl3)-induced memory impairment in rats along with biochemical mechanism of its protective action.
Memory deficiency was produced by AlCl3 (100 mg/kg; p.o.) in experimental animals. Learning and memory activity was measured using Morris water maze (MWM) test model. Central cholinergic activity was evaluated through the measurement of brain acetylcholinesterase (AChE) activity. In addition to the above, oxidative stress was determined through assessment of brain thiobarbituric acid-reactive species (TBARS) and glutathione (GSH) levels.
AlCl3 administration prompted significant deficiency of learning and memory in rats, as specified by a noticeable reduction in MWM presentation. AlCl3 administration also produced a significant deterioration in brain AChE action and brain oxidative stress (increase in TBARS and decrease in GSH) levels. Treatment with morusin (5.0 and 10.0 mg/kg, dose orally) significantly overturned AlCl3- induced learning and memory shortages along with diminution of AlCl3-induced rise in brain AChE activity and brain oxidative stress levels.
It may be concluded that morusin exerts a memory-preservative outcome in mental discrepancies of rats feasibly through its various activities.
大脑中铝含量升高具有神经毒性,可导致学习和记忆缺陷。在中医中,桑白皮被用作一种神经保护草药。本研究旨在探讨桑色素对三氯化铝(AlCl3)诱导的大鼠记忆损伤的恢复作用及其保护作用的生化机制。
在实验动物中,通过给予AlCl3(100mg/kg;口服)造成记忆缺陷。使用莫里斯水迷宫(MWM)测试模型测量学习和记忆活动。通过测量脑乙酰胆碱酯酶(AChE)活性来评估中枢胆碱能活性。除此之外,通过评估脑硫代巴比妥酸反应性物质(TBARS)和谷胱甘肽(GSH)水平来确定氧化应激。
如MWM表现明显降低所示,给予AlCl3会导致大鼠学习和记忆显著缺陷。给予AlCl3还会使脑AChE活性和脑氧化应激(TBARS升高和GSH降低)水平显著恶化。用桑色素(5.0和10.0mg/kg,口服给药)治疗可显著逆转AlCl3诱导的学习和记忆缺陷,同时减少AlCl3诱导的脑AChE活性升高和脑氧化应激水平。
可以得出结论,桑色素可能通过其多种活性在大鼠精神障碍中发挥记忆保护作用。