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首页> 外文期刊>Metabolic brain disease >Curcumin improves episodic memory in cadmium induced memory impairment through inhibition of acetylcholinesterase and adenosine deaminase activities in a rat model
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Curcumin improves episodic memory in cadmium induced memory impairment through inhibition of acetylcholinesterase and adenosine deaminase activities in a rat model

机译:姜黄素通过在大鼠模型中抑制乙酰胆碱酯酶和腺苷脱氨基酶活性,改善了镉诱导的记忆损伤中的情节内存

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摘要

Curcumin, the main polyphenolic component of turmeric (Curcuma longa) rhizomes has been reported to exert cognitive enhancing potential with limited scientific basis. Hence, this study sought to evaluate the effect of curcumin on cerebral cortex acetylcholinesterase (AChE) and adenosine deaminase (ADA) activities in cadmium (Cd)-induced memory impairment in rats. Animals were divided into six groups (n = 6): saline/vehicle, saline/curcumin 12.5 mg/kg, saline/curcumin 25 mg/kg, Cd/vehicle, Cd/curcumin 12.5 mg/kg, and Cd/curcumin 25 mg/kg. Rats received Cd (2.5 mg/kg) and curcumin (12.5 and 25 mg/kg, respectively) by gavage for 7 days. The results of this study revealed that cerebral cortex AChE and ADA activities were increased in Cd-poisoned rats, and curcumin co-treatment reversed these activities to the control levels. Furthermore, Cd intoxication increased the level of lipid peroxidation in cerebral cortex with a concomitant decreased in functional sulfuhydryl (-SH) group and nitric oxide (NO), a potent neurotransmitter and neuromodulatory agent. However, the co-treatment with curcumin at 12.5 and 25 mg/kg, respectively increased the non-enzymatic antioxidant status and NO in cerebral cortex with a decreased in malondialdehyde (MDA) level. Therefore, inhibition of AChE and ADA activities as well as increased antioxidant status by curcumin in Cd-induced memory dysfunction could suggest some possible mechanism of action for their cognitive enhancing properties.
机译:据报道,姜黄素,姜黄(Curcuma Longa)根茎的主要多酚组分促使认知增强潜力有限。因此,该研究试图评估姜黄素对大鼠镉(CD)诱导的大鼠内存损伤中的脑皮质乙酰乙酰胆碱酯酶(ACHE)和腺苷脱氨基酶(ADA)活性的影响。将动物分为六组(n = 6):盐水/载体,盐水/姜黄素12.5mg / kg,盐水/姜黄素25mg / kg,Cd /载体,Cd /姜黄素12.5mg / kg和Cd /姜黄素25mg /公斤。大鼠通过Gavage接受CD(2.5mg / kg)和姜黄素(分别为12.5和25mg / kg 7天。该研究的结果表明,CD中毒大鼠的脑皮质疼痛和ADA活性增加,姜黄素共同治疗将这些活动逆转到对照水平。此外,CD中毒增加了脑皮质中脂质过氧化水平,伴随亚磺铵(-SH)基团和一氧化氮(NO),有效的神经递质和神经调节剂。然而,在12.5和25mg / kg下用姜黄素的共处理分别增加了丙二醛(MDA)水平下降的非酶促抗氧化状态,并且在脑皮层中没有减少。因此,在CD诱导的记忆功能障碍中抑制ACHE和ADA活动以及姜黄素的抗氧化状态增加可能为其认知增强性能提出一些可能的作用机制。

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