Suppr超能文献

姜黄素(姜黄)对铝毒性的保护作用:对大鼠可能的行为和生化改变。

Protective effect of curcumin (Curcuma longa), against aluminium toxicity: Possible behavioral and biochemical alterations in rats.

机构信息

Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India.

出版信息

Behav Brain Res. 2009 Dec 28;205(2):384-90. doi: 10.1016/j.bbr.2009.07.012. Epub 2009 Jul 16.

Abstract

Aluminium is a potent neurotoxin and has been associated with Alzheimer's disease (AD) causality for decades. Prolonged aluminium exposure induces oxidative stress and increases amyloid beta levels in vivo. Current treatment modalities for AD provide only symptomatic relief thus necessitating the development of new drugs with fewer side effects. The aim of the study was to demonstrate the protective effect of chronic curcumin administration against aluminium-induced cognitive dysfunction and oxidative damage in rats. Aluminium chloride (100 mg/kg, p.o.) was administered to rats daily for 6 weeks. Rats were concomitantly treated with curcumin (per se; 30 and 60 mg/kg, p.o.) daily for a period of 6 weeks. On the 21st and 42nd day of the study behavioral studies to evaluate memory (Morris water maze and elevated plus maze task paradigms) and locomotion (photoactometer) were done. The rats were sacrificed on 43rd day following the last behavioral test and various biochemical tests were performed to assess the extent of oxidative damage. Chronic aluminium chloride administration resulted in poor retention of memory in Morris water maze, elevated plus maze task paradigms and caused marked oxidative damage. It also caused a significant increase in the acetylcholinesterase activity and aluminium concentration in aluminium treated rats. Chronic administration of curcumin significantly improved memory retention in both tasks, attenuated oxidative damage, acetylcholinesterase activity and aluminium concentration in aluminium treated rats (P<0.05). Curcumin has neuroprotective effects against aluminium-induced cognitive dysfunction and oxidative damage.

摘要

铝是一种有效的神经毒素,几十年来一直与阿尔茨海默病(AD)的因果关系有关。长期暴露于铝会导致体内氧化应激和淀粉样β水平升高。目前 AD 的治疗方法仅提供症状缓解,因此需要开发副作用更少的新药。本研究的目的是证明慢性姜黄素给药对大鼠铝诱导的认知功能障碍和氧化损伤的保护作用。每天给大鼠口服氯化铝(100mg/kg),持续 6 周。同时,大鼠连续 6 周每天口服姜黄素(本身;30 和 60mg/kg)。在研究的第 21 和 42 天,进行行为研究以评估记忆(莫里斯水迷宫和高架十字迷宫任务范式)和运动(光测计)。在最后一次行为测试后的第 43 天,处死大鼠,并进行各种生化测试以评估氧化损伤的程度。慢性氯化铝给药导致莫里斯水迷宫、高架十字迷宫任务范式中的记忆保留不良,并导致明显的氧化损伤。它还导致乙酰胆碱酯酶活性和铝浓度在铝处理大鼠中显著增加。慢性姜黄素给药显著改善了两种任务中的记忆保留,减轻了氧化损伤、乙酰胆碱酯酶活性和铝浓度在铝处理大鼠中的增加(P<0.05)。姜黄素对铝诱导的认知功能障碍和氧化损伤具有神经保护作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验