Beigom Hejaziyan Leila, Hosseini Seyed Mohammad, Taravati Ali, Asadi Mohammad, Bakhshi Mahyar, Moshaei Nezhad Pedram, Gol Mohammad, Mououdi Mobina
Cellular and Molecular Biology Research Center (CMBRC), Babol University of Medical Sciences, Babol, Iran.
Department of Human Anatomy, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran.
Evid Based Complement Alternat Med. 2023 Apr 10;2023:4926151. doi: 10.1155/2023/4926151. eCollection 2023.
The purpose of the current study is to investigate the effect of aquatic extract against the oxidative damage induced by aluminum chloride intoxication in Alzheimer's model of Wister rats. Rats were divided randomly into seven groups ( = 10). Control group received no treatment, sham group received distilled water orally, aluminum group (AL) was administered AlCl (100 mg/kg) orally, extract 1 and 2 groups were treated with only aqueous extract (DRE) (500 and 1000 mg/kg), and treatment 1 and 2 groups received aqueous extract (500 and 1000 mg/kg) and AlCl (100 mg/kg) orally. The brain tissues were sampled for histopathological examination, and biochemical analysis was conducted for estimating the enzyme activities of acetylcholinesterase and catalase (CAT), the levels of GSH and MDA, and ferric reducing antioxidant power. According to the results of behavioral tests, AL administration showed a reduction in spatial memory and remarkably increased the time needed for reaching the invisible platform. The administration of Al-induced oxidative stress and an increase of the enzyme activity of AChE. Al administration increased AChE level from 1.176 ± 0.173 to 3.62 ± 0.348, which was a significant rise. However, treating with the extract at the dose of 1000 mg/kg downregulated it to 1.56 ± 0.303. Administration of the extract caused an increased level of catalase and glutathione levels in treatment groups, attenuated MDA level, and regulated AChE activity. Our results illustrate that administration of extract has a protective effect against the oxidative damage induced by AlCl intoxication in Alzheimer's model.
本研究的目的是探讨水提取物对氯化铝中毒诱导的Wistar大鼠阿尔茨海默病模型氧化损伤的影响。将大鼠随机分为七组(每组n = 10)。对照组不接受任何处理,假手术组口服蒸馏水,铝组(AL)口服给予AlCl₃(100 mg/kg),提取物1组和2组仅用水提取物(DRE)(500和1000 mg/kg)处理,处理1组和2组口服给予水提取物(500和1000 mg/kg)和AlCl₃(100 mg/kg)。采集脑组织进行组织病理学检查,并进行生化分析以评估乙酰胆碱酯酶和过氧化氢酶(CAT)的酶活性、谷胱甘肽(GSH)和丙二醛(MDA)水平以及铁还原抗氧化能力。根据行为测试结果,给予AL显示空间记忆减退,并显著增加到达不可见平台所需的时间。给予Al诱导氧化应激并增加乙酰胆碱酯酶的酶活性。给予Al使乙酰胆碱酯酶水平从1.176±0.173增加到3.62±0.348,这是显著升高。然而,用1000 mg/kg剂量的提取物处理可将其下调至1.56±0.303。给予提取物导致处理组过氧化氢酶水平和谷胱甘肽水平升高,减轻MDA水平,并调节乙酰胆碱酯酶活性。我们的结果表明,给予提取物对氯化铝中毒诱导的阿尔茨海默病模型氧化损伤具有保护作用。