杉木对氯化铝诱发大鼠阿尔茨海默病的有益作用

Q4 Biochemistry, Genetics and Molecular Biology
Raju Asirvatham, Daiay Pa, S. Salam
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引用次数: 0

摘要

氯化铝(AlCl3)会引起大鼠的神经炎症,从而导致阿尔茨海默病的发展。目前的研究重点是众所周知的Rasna来源——柳叶草(PL)的氢乙醇提取物的抗阿尔茨海默病和抗氧化潜力。植物成分,如pluchine和moretenol乙酸酯被选择用于PASS在线和分子对接(在计算机中)实验模型。将36只Wistar大鼠分为VI组,每组6只。第一组:正常对照,第二组:疾病对照,第三组:利瓦斯的明(0.3 mg/kg,p.o),第四组和第五组:PL的水乙醇提取物(HMEPL,200 mg/kg,400 mg/kg,p.o.),第六组:Rasna阿育吠陀配方(AFR)(1ml/kg,p.o.o)。除第一组外,所有动物均给予氯化铝(AlCl3)(300 mg/kg,p.o.o.)。AlCl3和植物提取物治疗20天。在第0天、第7天、第14天和第20天,评估行为研究和体重变化。在第21天处死大鼠,分离它们的大脑,测量抗氧化酶水平、蛋白质水平和神经递质水平。研究了大脑皮层和海马部分的组织病理学。在第II组动物中,进入的次数、在闭合臂上花费的时间和登上极点所需的时间都增加了,但在用200mg/kg、400mg/kg和1ml/kg剂量的HMEPL和AFR治疗的组中,这一情况发生了逆转。在疾病对照组中,AlCl3(300mg/kg,p.o.)导致蛋白质含量增加1.5倍,丙二醛增加1.7倍,同样,在用HMEPL和AFR处理的组中,观察到体重减少1.3倍,超氧化物歧化酶减少2.2倍,过氧化氢酶减少3.3倍,谷胱甘肽水平增加3.1倍,并得到纠正和恢复。此外,组织病理学结果显示HMEPL和AFR提供了细胞水平的保护。HMEPL的活性成分被发现具有抗阿尔茨海默病和抗氧化潜力,并在计算机研究中得到证实。HMEPL>AFR是抗阿尔茨海默病和抗氧化作用的顺序。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The beneficial effect of Pluchea lanceolata on aluminum chloride-induced Alzheimer's disease in rats
Aluminum chloride (AlCl3) causes neuroinflammation in rats, which leads to the development of Alzheimer's disease. The current study focused on the anti-Alzheimer and antioxidant potential of hydromethanolic extracts of Pluchea lanceolata (PL), a well-known Rasna source. Phytoconstituents such as pluchine and moretenol acetate are selected for the PASS online and molecular docking (in silico) experimental model. A total of 36 Wistar rats were divided into VI groups, each with six rats. Group I: normal control, Group II: disease control, Group III: Rivastigmine (0.3 mg/kg, p.o), Group IV and V: Hydromethanolic extract of PL (HMEPL, 200 mg/kg, 400 mg/kg, p.o), and Group VI: Ayurvedic Formulation of Rasna (AFR) (1ml/kg, p.o). Except for group I, all of the animals were given Aluminum Chloride (AlCl3) (300 mg/kg, p.o). AlCl3 and plant extracts were given for 20day treatment. On the 0th, 7th, 14th, and 20th days, the behavioural study and changes in body weight were evaluated. Rats were sacrificed on the 21st day, their brains were separated, and antioxidant enzyme levels, protein levels, and neurotransmitter levels were measured. Histopathologies of the cortex and hippocampus parts of the brain were studied. The number of entries, as well as time spent in the closed arm and time taken to ascend the pole, were all increased in Group II animals, but this was reversed in groups treated with 200 mg/kg, 400 mg/kg, and1 ml/kg dosages of HMEPL and AFR. In the disease control group, AlCl3 (300 mg/kg, p.o.) caused a 1.5 fold increase in protein content and 1.7 fold increase in malondialdehyde, similarly, 1.3 fold reduction in body weight, 2.2 fold superoxide dismutase, 3.3 fold catalase, and 3.1 fold glutathione level were observed and were corrected and restored in groups treated with HMEPL and AFR. Furthermore, the histopathology findings revealed that HMEPL and AFR provided the cellular-level protection. The active components of HMEPL were found to have anti-Alzheimer and antioxidant potential and were confirmed in an in silico investigation. HMEPL > AFR was the order of anti-Alzheimer and antioxidant effectiveness.
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来源期刊
Journal of Cellular Neuroscience and Oxidative Stress
Journal of Cellular Neuroscience and Oxidative Stress Biochemistry, Genetics and Molecular Biology-Biophysics
CiteScore
1.10
自引率
0.00%
发文量
8
期刊介绍: Journal of Cellular Neuroscience and Oxidative Stress isan online journal that publishes original research articles, reviews and short reviews on themolecular basisofbiophysical,physiological and pharmacological processes thatregulate cellular function, and the control or alteration of these processesby theaction of receptors, neurotransmitters, second messengers, cation, anions,drugsor disease. Areas of particular interest are four topics. They are; 1. Ion Channels (Na+-K+Channels, Cl– channels, Ca2+channels, ADP-Ribose and metabolism of NAD+,Patch-Clamp applications) 2. Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) 3. Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD+ on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson’s and Alzheimer’s diseases) 4. Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)
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