Adenosine ameliorated Aβ25−35-induced brain injury through the inhibition of apoptosis and oxidative stress via an ERα pathway

Zeng, Mengnan; Feng, Aozi; Zhao, Chenxin; Zhang, Beibei; Guo, Pengli; Li, Meng; Zhang, Qinqin; Zhang, Yuhan; Fan, Ruixin; Lyu, Jun; Zheng, Xiaoke

doi:10.1016/j.brainres.2022.147944

Cited by 8 publications

(4 citation statements)

References 25 publications

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“…GSK3β inhibition was observed in response to trehalose, which upregulated ERα and ERβ and protected APP/PS1 mice against dietary advanced glycation end product (dAGE)-induced neurotoxicity and cognitive impairment [ 53 ]. Our results are also in line with the ERα-mediated anti-apoptotic effects of adenosine against Aβ 25-35 -induced brain damage [ 54 ] and of formononetin in AD patients [ 55 ], as well as the ER/PI3K/Akt-mediated effect of naringenin against Aβ 25-35 -caused damage in neuronally differentiated PC12 cells [ 56 ].…”

Section: Discussionsupporting

confidence: 86%

Posttreatment with PaPE-1 Protects from Aβ-Induced Neurodegeneration Through Inhibiting the Expression of Alzheimer’s Disease-Related Genes and Apoptosis Process That Involves Enhanced DNA Methylation of Specific Genes

Pietrzak-Wawrzyńska,

Wnuk,

Przepiórska-Drońska

et al. 2023

Mol Neurobiol

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Targeting the non-nuclear estrogen receptor (ER) signaling has been postulated as novel therapeutic strategy for central nervous system pathologies. Recently, we showed that newly designed PaPE-1 (Pathway Preferential Estrogen-1), which selectively activates ER non-nuclear signaling pathways, elicited neuroprotection in a cellular model of Alzheimer’s disease (AD) when it was applied at the same time as amyloid-β (Aβ). Since delayed treatment reflects clinical settings better than cotreatment does, current basic study proposes a novel therapeutic approach for AD that relies on a posttreatment with PaPE-1. In this study, mouse neuronal cell cultures treated with preaggregated Aβ1-42 (10 µM) showed the presence of extracellular Aβ1-42, confirming the adequacy of the AD model used. We are the first to demonstrate that a 24-h delayed posttreatment with PaPE-1 decreased the degree of Aβ-induced neurodegeneration, restored neurite outgrowth, and inhibited the expression of AD-related genes, i.e., Rbfox, Apoe, Bace2, App, and Ngrn, except for Chat, which was stimulated. In addition, PaPE-1 elicited anti-apoptotic effects by inhibiting Aβ-induced caspase activities as well as attenuating apoptotic chromatin condensation, and in these ways, PaPE-1 prevented neuronal cell death. Posttreatment with PaPE-1 also downregulated the Aβ-affected mRNA expression of apoptosis-specific factors, such as Bax, Gsk3b, Fas, and Fasl, except for Bcl2, which was upregulated by PaPE-1. In parallel, PaPE-1 decreased the protein levels of BAX, FAS, and FASL, which were elevated in response to Aβ. PaPE-1 elicited a decrease in the BAX/BCL2 ratio that corresponds to increased methylation of the Bax gene. However, the PaPE-1-evoked Bcl2 gene hypermethylation suggests other PaPE-1-dependent mechanisms to control Aβ-induced apoptosis.

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Section: Discussionsupporting

confidence: 86%

Posttreatment with PaPE-1 Protects from Aβ-Induced Neurodegeneration Through Inhibiting the Expression of Alzheimer’s Disease-Related Genes and Apoptosis Process That Involves Enhanced DNA Methylation of Specific Genes

Pietrzak-Wawrzyńska,

Wnuk,

Przepiórska-Drońska

et al. 2023

Mol Neurobiol

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“…Liquiritigenin has the ability to cure immunological dysfunction by increasing cAMP synthesis in several cell lines and controlling immune cell death [ 40 , 49 ]. Adenosine alleviated amyloid β-protein 25-35 -induced brain damage by preventing apoptosis and oxidative stress [ 50 ]. Naringenin may have anti-coronavirus disease 2019 (COVID-19) effects by inhibiting the COVID-19 major protease 3-chymotrypsin-like protease (3CLpro) and decreasing angiotensin converting enzyme receptor activation [ 51 ].…”

Section: Resultsmentioning

confidence: 99%

UPLC-QTOF-MS with a chemical profiling approach for holistic quality evaluation between a material reference of Wen Dan decoction and its commercial preparations

et al. 2023

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Background Wen Dan decoction (WDD) has been a famous classic formula for resolving phlegm since ancient times in China. Currently, there are many types of WDD commercial preparations produced through modern technology. However, it is not known whether the holistic quality of WDD commercial preparations is consistent with the traditional decocting method to exert its proper effects. Therefore, the WDD material reference was studied and prepared, which can represent the traditional Chinese formulation WDD. Methods A method based on UPLC-QTOF-MS was developed to evaluate the quality of WDD material reference and commercial prescriptions. At the same time, the multivariate statistical method was used to compare the differences between the material reference and the commercial prescription by principal component analysis (PCA) and heatmap. Finally, the UPLC-QTOF-MS method was established to quantitatively study 11 representative components, including naringin, hesperidin, neohesperidin, liquiritin, glycyrrhizic acid, adenosine, liquiritigenin, tangeretin, eriocitrin, naringenin and synephrine. Results A total of 107 compounds were identified in the WDD material reference by comparing the retention time and fragment ion characteristics, including 54 flavonoids, 14 triterpenes, 10 organic acids, 7 alkaloids, 7 coumarins and 15 other components. The samples were almost evenly split into two groups, indicating a difference in quality between the WDD material reference and its commercial preparations in multivariate statistical analysis. Eleven major components of linearity, precision, repeatability, stability and recovery rate met the requirements, which were clearly different in commercial preparations and WDD material references. In terms of the content of 11 components in the commercial preparation, only CP8 is close to the material reference, which is in agreement with the statistical analysis of the heatmap. The concentrations of naringin and neohesperidin from the WDD material reference were higher than those from the commercial preparations. Conclusions The quality evaluation method established in this study can be used to identify different sources of WDD but also proves that the WDD material reference contains higher naringin. Furthermore, this study confirmed that the preparation technology of WDD commercial prescriptions should be optimized on the basis of WDD material references, producing the closest possible clinical basis for the substance. Graphical Abstract

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“…After 24 h, A2 was replaced with another new object B, and the number of times the mice explored object A1 (TA1) and the new object B (TB) within 5 min was recorded. The preferential index was calculated as TB/(TA1 + TB), and the discrimination index was calculated as (TB‐TA1)/(TA1 + TB) (Cao et al, 2021; Zeng et al, 2022).…”

Section: Methodsmentioning

confidence: 99%

Futoquinol improves Aβ_25–35‐induced memory impairment in mice by inhibiting the activation of p38MAPK through the glycolysis pathway and regulating the composition of the gut microbiota

Zhang,

Chen,

Zeng

et al. 2024

Phytotherapy Research

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Futoquinol (Fut) is a compound extracted from Piper kadsura that has a nerve cell protection effect. However, it is unclear whether Fut has protective effects in Alzheimer's disease (AD). In this study, we aimed to explore the therapeutic effect of Fut in AD and its underlying mechanism. UPLC‐MS/MS method was performed to quantify Fut in the hippocampus of mice brain. The cognition ability, neuronal and mitochondria damage, and levels of Aβ1–42, Aβ1–40, p‐Tau, oxidative stress, apoptosis, immune cells, and inflammatory factors were measured in Aβ25–35‐induced mice. The content of bacterial meta‐geometry was predicted in the microbial composition based on 16S rDNA. The protein levels of HK II, p‐p38MAPK, and p38MAPK were detected. PC‐12 cells were cultured in vitro, and glucose was added to activate glycolysis to further explore the mechanism of action of Fut intervention in AD. Fut improved the memory and learning ability of Aβ25–35 mice, and reduced neuronal damage and the deposition of Aβ and Tau proteins. Moreover, Fut reduced mitochondrial damage, the levels of oxidative stress, apoptosis, and inflammatory factors. Fut significantly inhibited the expression of HK II and p‐p38MAPK proteins. The in vitro experiment showed that p38MAPK was activated and Fut action inhibited after adding 10 mM glucose. Fut might inhibit the activation of p38MAPK through the glycolysis pathway, thereby reducing oxidative stress, apoptosis, and inflammatory factors and improving Aβ25–35‐induced memory impairment in mice. These data provide pharmacological rationale for Fut in the treatment of AD.

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Adenosine ameliorated Aβ25−35-induced brain injury through the inhibition of apoptosis and oxidative stress via an ERα pathway

Cited by 8 publications

References 25 publications

Posttreatment with PaPE-1 Protects from Aβ-Induced Neurodegeneration Through Inhibiting the Expression of Alzheimer’s Disease-Related Genes and Apoptosis Process That Involves Enhanced DNA Methylation of Specific Genes

Posttreatment with PaPE-1 Protects from Aβ-Induced Neurodegeneration Through Inhibiting the Expression of Alzheimer’s Disease-Related Genes and Apoptosis Process That Involves Enhanced DNA Methylation of Specific Genes

UPLC-QTOF-MS with a chemical profiling approach for holistic quality evaluation between a material reference of Wen Dan decoction and its commercial preparations

Futoquinol improves Aβ_25–35‐induced memory impairment in mice by inhibiting the activation of p38MAPK through the glycolysis pathway and regulating the composition of the gut microbiota

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Adenosine ameliorated Aβ25−35-induced brain injury through the inhibition of apoptosis and oxidative stress via an ERα pathway

Cited by 8 publications

References 25 publications

Posttreatment with PaPE-1 Protects from Aβ-Induced Neurodegeneration Through Inhibiting the Expression of Alzheimer’s Disease-Related Genes and Apoptosis Process That Involves Enhanced DNA Methylation of Specific Genes

Posttreatment with PaPE-1 Protects from Aβ-Induced Neurodegeneration Through Inhibiting the Expression of Alzheimer’s Disease-Related Genes and Apoptosis Process That Involves Enhanced DNA Methylation of Specific Genes

UPLC-QTOF-MS with a chemical profiling approach for holistic quality evaluation between a material reference of Wen Dan decoction and its commercial preparations

Futoquinol improves Aβ25–35‐induced memory impairment in mice by inhibiting the activation of p38MAPK through the glycolysis pathway and regulating the composition of the gut microbiota

Contact Info

Product

Resources

About

Futoquinol improves Aβ_25–35‐induced memory impairment in mice by inhibiting the activation of p38MAPK through the glycolysis pathway and regulating the composition of the gut microbiota