Neuroprotective effects of Eriobotrya japonica against β-amyloid-induced oxidative stress and memory impairment

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the accumulation of β-amyloid plaques and hyperphosphorylated tau proteins in the brain. Cell signaling pathways such as PI3K/Akt are known to play an essential role in regulating cell survival, motility, transcription, metabolism, and progression of the cell cycle. Recent studies demonstrated that the disruption of these signaling pathways in neurodegenerative disorders leads to oxidative stress and cell death. Targeting these altered signaling pathways could be considered as the therapeutic approach for neurodegenerative disorders. Ginsenoside Rh1 is known to provide beneficial effects in various diseases such as cancer, diabetes, and inflammation. In this study, human neuroblastoma SH-SY5Y cells were treated with the β-amyloid oligomers alone or in combination with ginsenoside Rh1. We observed that ginsenoside Rh1 was able to attenuate β-amyloid induced oxidative stress and cell death by activating the PI3K/Akt signaling pathway. Based on these findings, we suggest that ginsenoside Rh1 might be an efficacious therapeutic agent for AD.

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Neuroprotective effects of berberine on recognition memory impairment, oxidative stress, and damage to the purinergic system in rats submitted to intracerebroventricular injection of streptozotocin

Psychopharmacology ◽

10.1007/s00213-018-5090-6 ◽

2018 ◽

Vol 236 (2) ◽

pp. 641-655 ◽

Cited By ~ 10

Author(s):

Juliana Sorraila de Oliveira ◽

Fátima Husein Abdalla ◽

Guilherme Lopes Dornelles ◽

Taís Vidal Palma ◽

Cristiane Signor ◽

...

Keyword(s):

Oxidative Stress ◽

Recognition Memory ◽

Memory Impairment ◽

Intracerebroventricular Injection ◽

Neuroprotective Effects ◽

Purinergic System

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Pyrola incarnata demonstrates neuroprotective effects against β-amyloid-induced memory impairment in mice

Bioorganic & Medicinal Chemistry Letters ◽

10.1016/j.bmcl.2019.126858 ◽

2020 ◽

Vol 30 (2) ◽

pp. 126858

Author(s):

Shuang-Jun Li ◽

Qian Liu ◽

Xiao-Bin He ◽

Jin-Ping Liu ◽

Xiao-Liu Liu ◽

...

Keyword(s):

Memory Impairment ◽

Neuroprotective Effects ◽

Β Amyloid

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Ficus erecta Thunb Leaves Alleviate Memory Loss Induced by Scopolamine in Mice via Regulation of Oxidative Stress and Cholinergic System

Molecular Neurobiology ◽

10.1007/s12035-021-02358-1 ◽

2021 ◽

Author(s):

Eunjin Sohn ◽

Yu Jin Kim ◽

Joo-Hwan Kim ◽

Soo-Jin Jeong

Keyword(s):

Oxidative Stress ◽

Cholinergic System ◽

Memory Impairment ◽

Neuronal Cell ◽

In Vitro Assays ◽

Drug Candidate ◽

Avoidance Task ◽

Related Factor ◽

Neuroprotective Effects

AbstractWe examined the neuropharmacological effects of ethanol extract of Ficus erecta Thunb leaves (EEFE) on cognitive dysfunction in a scopolamine (SCO)-induced memory impairment animal model. Memory impairment was measured using the Y-maze test and passive avoidance task (PAT). For 19 days, EEFE (100 or 200 mg/kg) was treated through oral administration. Treatment with EEFE ameliorated memory impairment in behavioral tests, along with significant protection from neuronal oxidative stress and neuronal cell loss in the brain tissues of SCO-injected mice. Antioxidant and neuroprotective effects of EEFE were further confirmed using in vitro assays. Our findings indicate that the mechanisms of neuroprotection and antioxidation of EEFE are regulated by the cholinergic system, promotion of cAMP response element-binding protein (CREB) phosphorylation, and the nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase (HO)-1 signaling activation. The current study proposes that EEFE could be an encouraging plant resource and serve as a potent neuropharmacological drug candidate against neurodegenerative diseases.

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Xanthohumol ameliorates memory impairment and reduces the deposition of β-amyloid in APP/PS1 mice via regulating the mTOR/LC3II and Bax/Bcl-2 signalling pathways

Journal of Pharmacy and Pharmacology ◽

10.1093/jpp/rgab052 ◽

2021 ◽

Author(s):

Xiao-Lei Sun ◽

Jia-Bao Zhang ◽

Yun-Xiang Guo ◽

Tian-Shuang Xia ◽

Ling-Chuan Xu ◽

...

Keyword(s):

Memory Impairment ◽

Biological Activities ◽

Signalling Pathways ◽

Neuroprotective Effects ◽

In Vivo Test ◽

Oxidative Markers ◽

Humulus Lupulus L ◽

Β Amyloid ◽

Apoptosis Proteins

Abstract Objectives Xanthohumol (XAN) is a unique component of Humulus lupulus L. and is known for its diverse biological activities. In this study, we investigated whether Xanthohumol could ameliorate memory impairment of APP/PS1 mice, and explored its potential mechanism of action. Methods APP/PS1 mice were used for in vivo test and were treated with N-acetylcysteine and Xanthohumol for 2 months. Learning and memory levels were evaluated by the Morris water maze. Inflammatory and oxidative markers in serum and hippocampus and the deposition of Aβ in the hippocampus were determined. Moreover, the expression of autophagy and apoptosis proteins was also evaluated by western blot. Key findings Xanthohumol significantly reduced the latency and increased the residence time of mice in the target quadrant. Additionally, Xanthohumol increased superoxide dismutase level and reduced Interleukin-6 and Interleukin-1β levels both in serum and hippocampus. Xanthohumol also significantly reduced Aβ deposition in the hippocampus and activated autophagy and anti-apoptotic signals. Conclusions Xanthohumol effectively ameliorates memory impairment of APP/PS1 mice by activating mTOR/LC3 and Bax/Bcl-2 signalling pathways, which provides new insight into the neuroprotective effects of Xanthohumol.

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Neuroprotective Effects ofCentella asiaticaagainst Intracerebroventricular Colchicine-Induced Cognitive Impairment and Oxidative Stress

International Journal of Alzheimer s Disease ◽

10.4061/2009/972178 ◽

2009 ◽

Vol 2009 ◽

pp. 1-8 ◽

Cited By ~ 36

Author(s):

Anil Kumar ◽

Samrita Dogra ◽

Atish Prakash

Keyword(s):

Oxidative Stress ◽

Cognitive Impairment ◽

Oxidative Damage ◽

Memory Impairment ◽

Memory Performance ◽

Centella Asiatica ◽

Acetylcholinesterase Activity ◽

Early Event ◽

Neuroprotective Effects ◽

Male Wistar Rats

Oxidative stress appears to be an early event involved in the pathogenesis of Alzheimer's disease. The present study was designed to investigate the neuroprotective effects ofCentella asiaticaagainst colchicine-induced memory impairment and oxidative damage in rats. Colchicine (15 μg/5 μL) was administered intracerebroventricularly in the lateral ventricle of male wistar rats. Morris water maze and plus-maze performance tests were used to assess memory performance tasks. Various biochemical parameters such as lipid peroxidation, nitrite, reduced glutathione, glutathione-S-transferase, superoxide dismutase, acetylcholinesterase were also assessed. ICV colchicine resulted marked memory impairment and oxidative damage. Chronic treatment withCentella asiaticaextract (150 and 300 mg/kg, p.o.) for a period of 25 days, beginning 4 days prior to colchicine administration, significantly attenuated colchicine-induced memory impairment and oxidative damage. Besides,Centella asiaticasignificantly reversed colchicines administered increase in acetylcholinesterase activity. Thus, present study indicates protective effect ofCentella asiaticaagainst colchicine-induced cognitive impairment and associated oxidative damage.

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β-Asarone Ameliorates β-Amyloid–Induced Neurotoxicity in PC12 Cells by Activating P13K/Akt/Nrf2 Signaling Pathway

Frontiers in Pharmacology ◽

10.3389/fphar.2021.659955 ◽

2021 ◽

Vol 12 ◽

Author(s):

Miaomiao Meng ◽

Lijuan Zhang ◽

Di AI ◽

Hongyun Wu ◽

Wei Peng

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Neuronal Damage ◽

Cell Model ◽

Cell Damage ◽

Neuroprotective Effects ◽

Akt Phosphorylation ◽

Nrf2 Signaling Pathway ◽

Amyloid Aβ ◽

Β Amyloid

Accumulation of β-amyloid (Aβ) causes oxidative stress, which is the major pathological mechanism in Alzheimer’s disease (AD). β-asarone could reduce Aβ-induced oxidative stress and neuronal damage, but the molecular mechanism remains elusive. In this study, we used an Aβ-stimulated PC12 cell model to explore the neuroprotective effects and potential mechanisms of β-asarone. The results showed that β-asarone could improve cell viability and weaken cell damage and apoptosis. β-asarone could also decrease the level of ROS and MDA; increase the level of SOD, CAT, and GSH-PX; and ameliorate the mitochondrial membrane potential. Furthermore, β-asarone could promote the expression of Nrf2 and HO-1 by upregulating the level of PI3K/Akt phosphorylation. In conclusion, β-asarone could exert neuroprotective effects by modulating the P13K/Akt/Nrf2 signaling pathway. β-asarone might be a promising therapy for AD.

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Marine Organisms as Alkaloid Biosynthesizers of Potential Anti-Alzheimer Agents

Marine Drugs ◽

10.3390/md20010075 ◽

2022 ◽

Vol 20 (1) ◽

pp. 75

Author(s):

Elisabete Lima ◽

Jorge Medeiros

Keyword(s):

Oxidative Stress ◽

Complex Disease ◽

Marine Organisms ◽

Neuroprotective Effects ◽

Amyloid Aβ ◽

Β Amyloid ◽

Amino Acid Tryptophan ◽

Τ Protein ◽

Derivatives Of ◽

Neuron Apoptosis

The incidence of neurodegenerative diseases, such as Alzheimer’s disease (AD), increases continuously demanding the urgent development of anti-Alzheimer’s agents. Marine organisms (MO) have to create their own defenses due to the adverse environment where they live and so synthesize several classes of compounds, such as akaloids, to defend themselves. Therefore, the identification of marine natural products with neuroprotective effects is a necessity. Being that AD is not only a genetic but also an environmental complex disease, a treatment for AD remains to discover. As the major clinical indications (CI) of AD are extracellular plaques formed by β-amyloid (Aβ) protein, intracellular neurofibrillary tangles (NFTs) formed by hyper phosphorylated τ-protein, uncommon inflammatory response and neuron apoptosis and death caused by oxidative stress, alkaloids that may decrease CI, might be used against AD. Most of the alkalolids with those properties are derivatives of the amino acid tryptophan mainly with a planar indole scaffold. Certainly, alkaloids targeting more than one CI, multitarget-directed ligands (MTDL), have the potential to become a lead in AD treatment. Alkaloids to have a maximum of activity against CI, should be planar and contain halogens and amine quaternization.

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