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Evaluation of anti-Alzheimer activity of Echinacea purpurea extracts in aluminum chloride-induced neurotoxicity in rat model

药理学 体内 神经毒性 胆碱酯酶 效力 神经炎症 海马体 丁酰胆碱酯酶 氧化应激 医学 毒性 阿切 乙酰胆碱酯酶 化学 体外 炎症 生物 生物化学 内科学 生物技术
作者
Salma Mostafa Mohamed,Mostafa Shalaby,Asmaa K. Al‐Mokaddem,Ahmed H. El-Banna,Hossny A. El-Banna,Ghazal Nabil
出处
期刊:Journal of Chemical Neuroanatomy [Elsevier BV]
卷期号:128: 102234-102234 被引量:8
标识
DOI:10.1016/j.jchemneu.2023.102234
摘要

Alzheimer's disease (AD) is one of the neurodegenerative illnesses that impair individual life & increase the demand for caregivers with no available curative medication right now. Therefore, there is a growing concern about employing herbal medicine to limit AD progression & improve patients' life quality, thus potentiating its add-on therapy. In addition, herbs are cost-effective & accessible with nearly no side effects. In the same vein, our study aimed to investigate the potency of Echinacea purpurea (EP) flower extracts to ameliorate the neurodegenerative effect of Aluminum chloride (AlCl3) in a rat model. Moreover, mechanistic studies, including impact on the cholinesterase activity, redox status, inflammatory mediators, behavior performance, glucose level & histopathology, were carried on. Our results showed that 250 mg/kg of Aqueous (AQ) & Alcoholic (AL) extracts of EP inhibited cholinesterase, restored oxidative balance, down-regulated IL-6 & TNF-α cytokines & improved behavior performance in vivo that was reflected in the brain picture by decreasing neuronal degeneration & amyloid plaques in cerebral cortex & hippocampus. The potency of both extracts was compared to reference drugs & AlCl3 positive control group. The AQ extract showed greater potency against COX-1, COX-2 & α-amylase in vitro, while the AL extract was more potent against cholinesterase in vitro, inflammatory cytokines, behavior & pathological improvement in vivo. Conclusively EP overcame AlCl3-induced neurobehavioral toxicity in the rat model via different pathways, which support its regular administration to postpone progressive neural damage in AD patients.
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