Effect of hesperidin extraction on cell proliferation and apoptosis of Alzheimer's disease induced by Aβ25–35

2010 ◽  
Author(s):  
Xiaoting Luo ◽  
Qin Huang ◽  
Shumei Li ◽  
Sisi Li ◽  
Liang Xiong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Proliferation ◽  
Proliferation And Apoptosis

Differential Expression of miR-381-3p in Alzheimer’s Disease Patients and Its Role in Beta-Amyloid-Induced Neurotoxicity and Inflammation

2021 ◽  
pp. 1-9
Author(s):  
Meng Zhang ◽  
Yonglei Liu ◽  
Pingping Teng ◽  
Qing Yang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Proliferation ◽  
Inflammatory Cytokines ◽  
Roc Curve ◽  
Pearson Correlation ◽  
Luciferase Reporter ◽  
Cell Models ◽  
Gene Assay ◽  
Proliferation And Apoptosis

<b><i>Introduction:</i></b> This study aimed to explore the diagnostic value and effect of miR-381-3p on Alzheimer’s disease (AD). <b><i>Methods:</i></b> RT-qPCR was used for the measurement of miR-381-3p levels. Pearson correlation coefficient was used for the correlation analysis. Receiver operating characteristic (ROC) curve was constructed to assess the distinct ability of miR-381-3p for AD. SH-SY5Y cells were treated with Aβ25-35 to establish an AD cell model. The role of miR-381-3p on cell proliferation and apoptosis was detected. ELISA was applied to detect the protein levels of inflammatory cytokine expression. The target relationship of miR-381-3p with PTGS2 was verified by luciferase reporter gene assay. <b><i>Results:</i></b> Low expression of miR-381-3p was detected in the serum of AD patients and cell models. There was a negative association of serum miR-381-3p with the serum inflammatory cytokines. The ROC curve demonstrated the distinct ability of serum miR-381-3p for AD, with the AUC value of 0.898, with a sensitivity of 87.5%, and a specificity of 77.7%. Overexpression of miR-381-3p reversed the influence of Aβ25-35 on cell proliferation and apoptosis, but miR-381-3p downregulation exacerbated the influence. miR-381-3p overexpression inhibited the release of IL-6, IL-1β, and TNF-α induced by Aβ25-35 treatment, whereas miR-381-3p downregulation further promoted the release of inflammatory cytokines. PTGS2 was the target gene of miR-381-3p and was upregulated in AD cell models. <b><i>Conclusion:</i></b> miR-381-3p is less expressed in the serum of AD patients and has potential diagnostic values for AD. Overexpression of miR-381-3p may attenuate Aβ25-35-induced neurotoxicity and inflammatory responses via targeting PTGS2 in SH-SY5Y cells.

scholarly journals Aβ-Induced Repressor Element 1-Silencing Transcription Factor (REST) Gene Delivery Suppresses Activation of Microglia-Like BV-2 Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Tongya Yu ◽  
Hui Quan ◽  
Yuzhen Xu ◽  
Yunxiao Dou ◽  
Feihong Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Proliferation ◽  
Transcription Factor ◽  
Cell Activation ◽  
Type I ◽  
Hairpin Rna ◽  
Cell Dysfunction ◽  
Repressor Element

Compelling evidence from basic molecular biology has demonstrated the crucial role of microglia in the pathogenesis of Alzheimer’s disease (AD). Microglia were believed to play a dual role in both promoting and inhibiting Alzheimer’s disease progression. It is of great significance to regulate the function of microglia and make them develop in a favorable way. In the present study, we investigated the function of repressor element 1-silencing transcription factor (REST) in Aβ1-42-induced BV-2 cell dysfunction. We concluded that Aβ1-42 could promote type I activation of BV-2 cells and induce cell proliferation, migration, and proinflammation cytokine TNF-α, IL-1β, and IL-6 expression. Meanwhile, REST was upregulated, and nuclear translocalization took place due to Aβ1-42 stimulation. When REST was knocked down by a specific short hairpin RNA (sh-RNA), BV-2 cell proliferation, migration, and proinflammation cytokine expression and secretion induced by Aβ1-42 were increased, demonstrating that REST may act as a repressor of microglia-like BV-2 cell activation.

Cell proliferation and neurogenesis alterations in Alzheimer’s disease and diabetes mellitus mixed murine models

2020 ◽  
Vol 154 (6) ◽  
pp. 673-692 ◽  
Author(s):  
Carmen Hierro‐Bujalance ◽  
Angel Marco ◽  
Juan José Ramos‐Rodríguez ◽  
Carmen Infante‐Garcia ◽  
Sara Bella Gomez‐Santos ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Proliferation ◽  
Murine Models

scholarly journals MiR-29c-3p May Promote the Progression of Alzheimer’s Disease through BACE1

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yanqun Cao ◽  
Xiangxiang Tan ◽  
Quzhe Lu ◽  
Kai Huang ◽  
Xiaoer Tang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Proliferation ◽  
Animal Models ◽  
Binding Sites ◽  
Target Genes ◽  
Specific Binding ◽  
Cell Models ◽  
Proliferation Activity ◽  
Bace1 Level

The aim of this study was to explore the specific role of miR-29c-3p in Alzheimer’s disease (AD). Animal models of AD were established by injecting streptozotocin (STZ) into mice through the lateral ventricle, while cell models of AD were induced by 10 μM β-amyloid (Aβ). We detected miR-29c-3p and β-site amyloid precursor protein cleaving enzyme 1 (BACE1) contents and measured AD cell proliferation and apoptosis. A low miR-29c-3p level and a high BACE1 level were detected in the brain tissue of AD animal models and AD cell models. Aβ-processed cells had markedly lower proliferation activity, higher apoptosis, increased phosphorylation of tau protein was over phosphorylated, but the overexpression of miR-29c-3p or the silencing of BACE1 significantly enhanced the cell proliferation activity and reduced cell apoptosis by regulating the contents of related proteins. Inhibition of miR-29c-3p or overexpression of BACE1 aggravated Aβ-induced side effects. We used Targetscan7.2 to predict the downstream target genes of miR-29c-3p. Then, we detected that there were target binding sites between miR-29c-3p and BACE1. The rescue experiment identified BACE1 as a functional target for miR-29c-3p. AD leads to decreased miR-29c-3p level and increased BACE1 level. MiR-29c-3p has specific binding sites with the 3′-untranslated region (3′-UTR) of BACE1 and thus negatively regulates the BACE1 level, thereby affecting the progression of AD.

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