Effect of microRNA-186 on oxidative stress injury of neuron by targeting interleukin 2 through the janus kinase-signal transducer and activator of transcription pathway in a rat model of Alzheimer's disease.

摘要: Recent studies have proposed that microRNAs (miR) function as novel diagnostic and prognostic biomarkers therapeutic targets in Alzheimer's disease (AD), a common among the elderly. In current study, we aim to explore effect of miR-186 on oxidative stress injury neuron rat models of AD with involvement interleukin-2 (IL2) Janus kinase/signal transducers activators transcription (JAK-STAT) pathways. AD were established, dual-luciferase reporter assay online software used confirm targeting relationship between IL2. Immunohistochemistry was used evaluating positive rate Afterward, define role AD, miR-186, IL2, JAK-STAT related protein (JAK2, STAT3) expressions quantified. Cell proliferation measured by 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide, cell apoptosis detected flow cytometry. We observed downregulated IL2 upregulated signaling pathway genes AD. The overexpression shown significantly promote while suppressing along expression protein. Collectively, key findings obtained from study potential an inhibitor development downregulation through suppression pathway.