Melatonin Rescue Oxidative Stress-Mediated Neuroinflammation/ Neurodegeneration and Memory Impairment in Scopolamine-Induced Amnesia Mice Model

Tahir, Muhammad; Ali, Tahir; Ikram, Muhammad; Khan, Amjad; Alam, Sayed Ibrar; Kim, Myeong Ok

doi:10.1007/s11481-018-9824-3

Cited by 151 publications

(102 citation statements)

References 68 publications

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“…Because the constituents of EEI have antioxidant properties, EEI may effectively ameliorate neuronal cell death by reducing reactive oxygen species, such as those generated by H 2 O 2 or Aβ1-42. Collectively, the results of the AChE and BACE1 inhibition assay coupled with those of the ABTS inhibition assay demonstrate that EEI has potent enzyme inhibition effects and antioxidant activity; these beneficial effects were further evaluated in vivo.We next conducted a passive avoidance and Morris water maze to investigate the memory-improving effect of EEI in an animal model of learning and memory deficits induced by SCO injection.Previous studies showed that memory impairment induced by SCO, a nonselective muscarinic receptor antagonist, is related to the oxidative stress and synaptic dysfunction, which plays an integral role in neurodegenerative disorders(Muhammad et al, 2019). Our study showed that EEI treatment significantly improved step-through latency in passive avoidance and escape latency in the maintenance training of the Morris water maze in SCO-induced memory deficit mice.…”

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confidence: 60%

“…We next conducted a passive avoidance and Morris water maze to investigate the memory‐improving effect of EEI in an animal model of learning and memory deficits induced by SCO injection. Previous studies showed that memory impairment induced by SCO, a nonselective muscarinic receptor antagonist, is related to the oxidative stress and synaptic dysfunction, which plays an integral role in neurodegenerative disorders (Muhammad et al, ). Our study showed that EEI treatment significantly improved step‐through latency in passive avoidance and escape latency in the maintenance training of the Morris water maze in SCO‐induced memory deficit mice.…”

Section: Discussionmentioning

confidence: 99%

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Memory‐enhancing effects ofIshige foliaceaextract: In vitro and in vivo study

et al. 2020

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Ishige foliacea is used as a functional food in East‐Asian countries. We evaluated the memory‐enhancing effect of an ethanol extract of I. foliacea (EEI) using in vitro and in vivo models. In vitro acetylcholinesterase and β‐secretase inhibitory activities, antioxidant properties, and neuroprotective effects against human neuronal cell death by H2O2 and β‐amyloid (Aβ) were investigated. We explored the memory‐enhancing effect and its underlying mechanism in a mouse model of scopolamine (SCO)‐induced memory deficits. EEI showed free radical scavenging and acetylcholinesterase and β‐secretase inhibition activities. Additionally, EEI significantly decreased neuronal cell death induced by H2O2 or Aβ in human neuroblastoma SH‐SY5Y cells. In behavior tests, SCO‐induced memory deficits was improved by EEI administration. EEI increased the protein expression of brain‐derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) and phosphorylated extracellular signal‐regulated kinase, which are related to synaptic plasticity in the hippocampus. EEI may ameliorate memory deficits and prevent neurodegenerative disorders. Practical applications As the population ages, dementia, a neurodegenerative disease, is becoming an important problem. Various Alzheimer's drugs have been developed based on the disease mechanism, but alternative treatments are required because of the low bioavailability and hepatotoxicity of current medications. Ishige foliacea is a type of brown algae containing various bioactive substances. Phlorotannins, known as brown algae polyphenols, have been studied for their various functionalities such as, anticancer, anti‐obesity, antioxidant, and sleep improvement effects, and have attracted attention as raw materials for developing new natural products. We found that the EEI mitigates SCO‐induced damage by protecting neurons from oxidative stress‐induced cell damage, controlling synthesis mechanisms of the causative agents of AD, and activating BDNF–TrkB–ERK signaling to promote memory function in the hippocampus. The results of this study can serve as a foundation for further research. Additionally, I. foliacea may be useful for treating and improving AD.

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confidence: 60%

Section: Discussionmentioning

confidence: 99%

Memory‐enhancing effects ofIshige foliaceaextract: In vitro and in vivo study

et al. 2020

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“…Sections were then permeabilized and incubated with blocking solution containing the Iba-1 antibody (1:100, Abcam) overnight at 4°C. The sections were then stained with a fluorophore-conjugated secondary antibody (1:1,000, CST) for 1 h, followed by 4′6-diamino-2-phenylindole (DAPI, Sigma) staining for another 1 h. Images were acquired by a fluorescence microscope Model DMi8 (Leica, Germany) and quantified using ImageJ software (National Institutes of Health) (Muhammad et al, 2019).…”

Section: Immunofluorescencementioning

confidence: 99%

Systems Pharmacology Approach to Investigate the Mechanism of Kai-Xin-San in Alzheimer’s Disease

Luo

Liao

et al. 2020

Front. Pharmacol.

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Alzheimer's disease (AD) is a complex neurodegenerative disease characterized by cognitive dysfunction. Kai-Xin-San (KXS) is a traditional Chinese medicine (TCM) formula that has been used to treat AD patients for over a thousand years in China. However, the therapeutic mechanisms of KXS for treating AD have not been fully explored. Herein, we used a comprehensive network pharmacology approach to investigate the mechanism of action of KXS in the treatment of AD. This approach consists of construction of multiple networks and Gene Ontology enrichment and pathway analyses. Furthermore, animal experiments were performed to validate the predicted molecular mechanisms obtained from the systems pharmacology-based analysis. As a result, 50 chemicals in KXS and 39 AD-associated proteins were identified as major active compounds and targets, respectively. The therapeutic mechanisms of KXS in treating AD were primarily related to the regulation of four pathology modules, including amyloid beta metabolism, tau protein hyperphosphorylation process, cholinergic dysfunction, and inflammation. In scopolamine-induced cognitive dysfunction mice, we validated the anti-inflammatory effects of KXS on AD by determining the levels of inflammation cytokines including interleukin (IL)-6, IL-1b, and tumor necrosis factor (TNF)-a. We also found cholinergic system dysfunction amelioration of KXS is correlated with upregulation of the cholinergic receptor CHRNB2. In conclusion, our work proposes a comprehensive systems pharmacology approach to explore the underlying therapeutic mechanism of KXS for the treatment of AD.

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“…Immunofluorescence staining was carried out according to standard protocols [39,40]. The slides were dried at room temperature overnight and washed with 0.1 M PBS two times for 10 min.…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

Oral Administration of Alpha Linoleic Acid Rescues Aβ-Induced Glia-Mediated Neuroinflammation and Cognitive Dysfunction in C57BL/6N Mice

Ali

Ikram

Park

et al. 2020

Cells

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In this work, we evaluated the effects of alpha linoleic acid (ALA), an omega-3 polyunsaturated fatty acid, on amyloid-beta-induced glial-cell-mediated neuroinflammation, amyloidogenesis, and cognitive dysfunction in mice. After an infusion of Aβ1–42 (Aβ1–42, 5 μL/5 min/mouse, intracerebroventricular injection (i.c.v), and respective treatments of ALA (60 mg/kg per oral for six weeks), neuroinflammation, apoptotic markers, and synaptic markers were evaluated by Western blot and immunofluorescence analyses. According to our findings, the infusion of Aβ1–42 activated Toll-like receptor 4 (TLR4), glial fibrillary acidic protein (GFAP), and ionized calcium adaptor molecule 1 (Iba-1) in the frontal cortices and hippocampi of the Aβ1–42-injected mice to a greater extent than the Aβ1–42 + ALA-cotreated mice. Similarly, there was an elevated expression of phospho-c-Jun-N-terminal kinase (p-JNK), phospho-nuclear factor-kB p65 (p-NF-kB p65 (Ser536)), and tissue necrosis factor (TNF) in the Aβ1–42 infused mouse brains; interestingly, these markers were significantly reduced in the Aβ + ALA-cotreated group. The elevated expression of pro-apoptotic markers was observed during apoptotic cell death in the Aβ1–42-treated mouse brains, whereas these markers were markedly reduced in the Aβ + ALA-cotreated group. Moreover, Aβ1–42 infusion significantly increased amyloidogenesis, as assessed by the enhanced expression of the amyloid precursor proteins (APP) beta-amyloid cleaving enzyme-1 (BACE-1) and amyloid-beta (Aβ1–42) in the mouse brains, whereas these proteins were markedly reduced in the Aβ + ALA-cotreated group. We also checked the effects of ALA against Aβ-triggered synaptic dysfunction and memory dysfunction, showing that ALA significantly improved memory and synaptic functions in Aβ-treated mouse brains. These results indicated that ALA could be an applicable intervention in neuroinflammation, apoptotic cell loss, amyloidogenesis, and memory dysfunction via the inhibition of TLR4 and its downstream targets in Aβ + ALA-cotreated mouse brains.

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Melatonin Rescue Oxidative Stress-Mediated Neuroinflammation/ Neurodegeneration and Memory Impairment in Scopolamine-Induced Amnesia Mice Model

Cited by 151 publications

References 68 publications

Memory‐enhancing effects ofIshige foliaceaextract: In vitro and in vivo study

Memory‐enhancing effects ofIshige foliaceaextract: In vitro and in vivo study

Systems Pharmacology Approach to Investigate the Mechanism of Kai-Xin-San in Alzheimer’s Disease

Oral Administration of Alpha Linoleic Acid Rescues Aβ-Induced Glia-Mediated Neuroinflammation and Cognitive Dysfunction in C57BL/6N Mice

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