Ameliorative effects of bromelain on aluminum-induced Alzheimer's disease in rats through modulation of TXNIP pathway

Eraky, Salma M.; Ramadan, Nehal M.; El-Magd, Nada F. Abo

doi:10.1016/j.ijbiomac.2022.11.291

Cited by 11 publications

(5 citation statements)

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“…In contrast to the control group, (ALZ) group in the current study displayed histopathological abnormalities that were de ned by a reduction in cell density, the deposition of amyloid plaques (AP) and neuro brillary tangles (NFTs), in both, the CA1 region of the hippocampus, and the cortex. Results reported in previous studies, exposition to D-gal/AlCl 3 showed cognitive impairments and marked neuronal loss in hippocampal conus ammonis 1 (CA1) [36][37]. Chronic honey administration signi cantly decreased hippocampus and cortical atrophy and neuronal death when administered at 150 mg/kg and 300 mg/kg.…”

Section: Discussionmentioning

confidence: 80%

Chestnut ‘castanea sativa mill.’ honey potential in preventing memory decline on alzheimer’s disease model mice: in vitro enzyme activities, behavioural, memorial and histopathological studies

djebli,

YAGOUB,

OSKAY

et al. 2024

Preprint

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The primary purpose of this research is to investigate, both in vitro and in vivo studies, whether Chestnut 'Castanea sativa Mill.' Honey consumption, can counteract the neurodegeneration occurring in Alzheimer's model mice brains caused by aluminium chloride combined with D-galactose. Within the scope of in vitro studies. The antioxidant activity of chestnut honey at a non-toxic concentration was then evaluated by DPPH and CUPRAC methods, indicating its radical scavenging and copper (II) ion reduction abilities, respectively. Finally, the modified Ellman method was used to measure its anti-acetylcholinesterase activity. For the in vivo studies, two chestnut honey doses were used, 150 mg/kg and 300mg/kg. As for the neurodegeneration, it was induced by Aluminium chloride at 100 mg/kg combined with D-galactose at 120 mg/kg. Following the neurological tests, the brain were subjected to histopathological study. The dose of chestnut honey, which has no effect on fibroblast cell growth following the 24-hour treatment was detected as 0.25% -w/v-, this dose was used for further in vitro assays. DPPH scavenging activity of the honey was 10.98 ± 1.20 g/mL -IC50-, while CUPRAC value was 0.57 ± 0.27 mM TEAC/g. The neurological tests, reported significant positive improvement in learning ability, these results were confirmed by the histopathological findings, in which the tissues section taken from the brain showed that, the honey markedly reduced hippocampal atrophy and neuronal loss. The results suggests that Chestnut honey acceptable daily-inake can reduce the burden of Alzheimer's disease, by preventingmemory impairment and brain alteration.

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Section: Discussionmentioning

confidence: 80%

Chestnut ‘castanea sativa mill.’ honey potential in preventing memory decline on alzheimer’s disease model mice: in vitro enzyme activities, behavioural, memorial and histopathological studies

djebli,

YAGOUB,

OSKAY

et al. 2024

Preprint

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“…This form of diabetes is characterized by decreased insulin signaling in the CNS and cognitive deficit [ 3 ]. This concept was further confirmed and developed [ 4 , 5 , 6 , 7 ]. It has been established that impaired glucose homeostasis in the brain caused by central IR is one of the important causes of neuronal death and impaired synaptic plasticity in AD [ 8 , 9 , 10 ].…”

Section: Introductionmentioning

confidence: 83%

Hot Spots for the Use of Intranasal Insulin: Cerebral Ischemia, Brain Injury, Diabetes Mellitus, Endocrine Disorders and Postoperative Delirium

Zorina

Derkach

2023

IJMS

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A decrease in the activity of the insulin signaling system of the brain, due to both central insulin resistance and insulin deficiency, leads to neurodegeneration and impaired regulation of appetite, metabolism, endocrine functions. This is due to the neuroprotective properties of brain insulin and its leading role in maintaining glucose homeostasis in the brain, as well as in the regulation of the brain signaling network responsible for the functioning of the nervous, endocrine, and other systems. One of the approaches to restore the activity of the insulin system of the brain is the use of intranasally administered insulin (INI). Currently, INI is being considered as a promising drug to treat Alzheimer’s disease and mild cognitive impairment. The clinical application of INI is being developed for the treatment of other neurodegenerative diseases and improve cognitive abilities in stress, overwork, and depression. At the same time, much attention has recently been paid to the prospects of using INI for the treatment of cerebral ischemia, traumatic brain injuries, and postoperative delirium (after anesthesia), as well as diabetes mellitus and its complications, including dysfunctions in the gonadal and thyroid axes. This review is devoted to the prospects and current trends in the use of INI for the treatment of these diseases, which, although differing in etiology and pathogenesis, are characterized by impaired insulin signaling in the brain.

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“…Previous studies have shown that TXNIP as an endogenous inhibitor of antioxidant thioredoxin was found to increase in AD patients and AD mouse models, and could be a key coordinator of different pathological processes ( Tsubaki et al, 2020 ). TXNIP connects oxidative stress and inflammation by interaction with the nucleotide-binding domain, leucine-rich-containing family, and pyrin domain-containing-3 (NLRP3) inflammasome complex ( Wang et al, 2019 ; Eraky and Ramadan, 2022 ; Sbai et al, 2022 ). Recent studies also suggested that blocking the interaction of NLRP3 provides a significant effect, and thus TXNIP could serve as a therapeutic target ( Zhang et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of diagnostic biomarkers in Alzheimer’s disease by integrated bioinformatic analysis and machine learning strategies

Jin

Cheng

Fei

et al. 2023

Front. Aging Neurosci.

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BackgroundAlzheimer’s disease (AD) is the most prevalent form of dementia, and is becoming one of the most burdening and lethal diseases. More useful biomarkers for diagnosing AD and reflecting the disease progression are in need and of significance.MethodsThe integrated bioinformatic analysis combined with machine-learning strategies was applied for exploring crucial functional pathways and identifying diagnostic biomarkers of AD. Four datasets (GSE5281, GSE131617, GSE48350, and GSE84422) with samples of AD frontal cortex are integrated as experimental datasets, and another two datasets (GSE33000 and GSE44772) with samples of AD frontal cortex were used to perform validation analyses. Functional Correlation enrichment analyses were conducted based on Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and the Reactome database to reveal AD-associated biological functions and key pathways. Four models were employed to screen the potential diagnostic biomarkers, including one bioinformatic analysis of Weighted gene co-expression network analysis (WGCNA)and three machine-learning algorithms: Least absolute shrinkage and selection operator (LASSO), support vector machine-recursive feature elimination (SVM-RFE) and random forest (RF) analysis. The correlation analysis was performed to explore the correlation between the identified biomarkers with CDR scores and Braak staging.ResultsThe pathways of the immune response and oxidative stress were identified as playing a crucial role during AD. Thioredoxin interacting protein (TXNIP), early growth response 1 (EGR1), and insulin-like growth factor binding protein 5 (IGFBP5) were screened as diagnostic markers of AD. The diagnostic efficacy of TXNIP, EGR1, and IGFBP5 was validated with corresponding AUCs of 0.857, 0.888, and 0.856 in dataset GSE33000, 0.867, 0.909, and 0.841 in dataset GSE44770. And the AUCs of the combination of these three biomarkers as a diagnostic tool for AD were 0.954 and 0.938 in the two verification datasets.ConclusionThe pathways of immune response and oxidative stress can play a crucial role in the pathogenesis of AD. TXNIP, EGR1, and IGFBP5 are useful biomarkers for diagnosing AD and their mRNA level may reflect the development of the disease by correlation with the CDR scores and Breaking staging.

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Ameliorative effects of bromelain on aluminum-induced Alzheimer's disease in rats through modulation of TXNIP pathway

Cited by 11 publications

References 74 publications

Chestnut ‘castanea sativa mill.’ honey potential in preventing memory decline on alzheimer’s disease model mice: in vitro enzyme activities, behavioural, memorial and histopathological studies

Chestnut ‘castanea sativa mill.’ honey potential in preventing memory decline on alzheimer’s disease model mice: in vitro enzyme activities, behavioural, memorial and histopathological studies

Hot Spots for the Use of Intranasal Insulin: Cerebral Ischemia, Brain Injury, Diabetes Mellitus, Endocrine Disorders and Postoperative Delirium

Identification of diagnostic biomarkers in Alzheimer’s disease by integrated bioinformatic analysis and machine learning strategies

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