4.5 Article

Neuroprotective effects of miR-331-3p through improved cell viability and inflammatory marker expression: Correlation of serum miR-331-3p levels with diagnosis and severity of Alzheimer's disease

期刊

EXPERIMENTAL GERONTOLOGY
卷 144, 期 -, 页码 -

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2020.111187

关键词

Alzheimer's disease; MicroRNA-331-3p; Cell viability; Inflammation; Diagnosis; Mini-mental state examination score

资金

  1. Project of Zibo City Key Research and Development Program [2019gy010103]

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The study found that the expression of miR-331-3p was significantly downregulated in AD patients and Aβ(1-40) treated SH-SY5Y cells. Serum miR-331-3p showed diagnostic potential and was correlated with MMSE scores and serum proinflammatory cytokine levels in AD patients. Overexpression of miR-331-3p in Aβ(1-40) treated SH-SY5Y cells enhanced cell viability and inhibited inflammatory responses, indicating a potential neuroprotective role of miR-331-3p.
Background: Alzheimer's disease (AD) is a common neurodegenerative disease with an increasing incidence rate. Numerous microRNAs (miRNAs) have been found to be involved in AD progression. This study aimed to investigate the expression and diagnostic value of microRNA-331-3p (miR-331-3p) in AD patients and to explore the effects of miR-331-3p on neuronal viability and neuminflammation. Methods: This study recruited AD patients and used A beta(1-40) treated SH-SY5Y cells mimicking AD characteristics. The expression of miR-331-3p was estimated using reverse transcription quantitative PCR. A receiver operating characteristic (ROC) analysis was used to evaluate the diagnostic value of miR-331-3p, and the correlation of miR-331-3p with patients' Mini-Mental State Examination (MMSE) scores and serum proinflammatory cytokines were analyzed. The effects of miR-331-3p on neuronal viability and inflammatory response were explored in SH-SY5Y cells by in vitro analysis. Results: In AD patients and A beta(1-40) treated SH-SY5Y cells, the expression of miR-331-3p was significantly downregulated. Serum miR-331-3p had certain diagnostic potential and was correlated with the MMSE scores and serum proinflammatory cytokine levels of AD patients. In A beta(1-40)-treated SH-SY5Y cells, the overexpression of miR-331-3p enhanced cell viability and inhibited inflammatory responses. Conclusion: The data of this study indicated that serum expression of miR-331-3p is decreased in AD patients, and is correlated with the MMSE scores and proinflammatory cytokine levels of AD patients. In addition, miR-331-3p can regulate the cell viability and the expression of pm-inflammatory cytokines of A beta(1-40) treated SH-SY5Y cells, indicating the potential neumprotective role of miR-331-3p.

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