John Jessy, Nampoothiri Madhavan, Kumar Nitesh, Mudgal Jayesh, Nampurath Gopalan Kutty, Chamallamudi Mallikarjuna Rao
Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, Karnataka, India.
Pharmacogn Mag. 2015 Apr-Jun;11(42):327-36. doi: 10.4103/0973-1296.153086.
Sesame oil from the seeds of Sesamum indicum Linn. (Pedaliaceae) has been used traditionally in Indian medical practice of Ayurveda in the treatment of central nervous system disorders and insomnia. A few published reports favor the anti-dementia effect of sesamol (SML), an active constituent of sesame oil.
Thus, the present study was aimed to explore the anti-dementia effect and possible mechanism (s) of SML in aluminium chloride (AlCl3)-induced cognitive dysfunction model in rodents with special emphasis on memory centers viz., hippocampus and frontal cortex.
Male Wistar rats were exposed to AlCl3 (175 mg/kg p.o.) for 60 days. SML (10 and 20 mg/kg) and rivastigmine (1 mg/kg) were administered orally 45 min before administration of AlCl3 for 60 days. Spatial memory was assessed using Morris water maze test. After 60 days of treatment animals were sacrificed, hippocampus and frontal cortex were collected and analyzed for acetylcholinesterase (AChE) activity, tumor necrosis factor (TNF-α) level, antioxidant enzymes (Glutathione, catalase), lipid peroxidation, and nitrite level. The circulating triglycerides, total cholesterol, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) levels were also analyzed.
SML significantly prevented behavioral impairments in aluminium-exposed rats. Treatment with SML reversed the increased cholesterol, triglycerides and LDL while raised the HDL levels. SML significantly corrected the effect of AlCl3 on AChE activity. Further, SML reversed the elevated nitric oxide, TNF-α and reduced antioxidant enzymes in hippocampus and frontal cortex.
The present study suggests the neuro-protection by SML against cognitive dysfunction induced by environmental toxin (AlCl3) in hippocampus and frontal cortex.
芝麻(脂麻科)种子中的芝麻油在印度阿育吠陀医学实践中传统上用于治疗中枢神经系统疾病和失眠。一些已发表的报告支持芝麻油的活性成分芝麻酚(SML)的抗痴呆作用。
因此,本研究旨在探讨SML在氯化铝(AlCl3)诱导的啮齿动物认知功能障碍模型中的抗痴呆作用及可能机制,特别关注记忆中枢,即海马体和额叶皮质。
雄性Wistar大鼠暴露于AlCl3(175mg/kg口服)60天。在给予AlCl3前45分钟口服给予SML(10和20mg/kg)和卡巴拉汀(1mg/kg),持续60天。使用莫里斯水迷宫试验评估空间记忆。治疗60天后处死动物,收集海马体和额叶皮质并分析乙酰胆碱酯酶(AChE)活性、肿瘤坏死因子(TNF-α)水平、抗氧化酶(谷胱甘肽、过氧化氢酶)、脂质过氧化和亚硝酸盐水平。还分析了循环甘油三酯、总胆固醇、低密度脂蛋白(LDL)和高密度脂蛋白(HDL)水平。
SML显著预防了铝暴露大鼠的行为障碍。SML治疗可逆转升高的胆固醇、甘油三酯和LDL水平,同时提高HDL水平。SML显著纠正了AlCl3对AChE活性的影响。此外,SML逆转了海马体和额叶皮质中一氧化氮、TNF-α升高以及抗氧化酶降低的情况。
本研究表明SML对海马体和额叶皮质中由环境毒素(AlCl3)诱导的认知功能障碍具有神经保护作用。