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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

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Journal of Cellular Physiology

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--- - |2 Recent studies have proposed that microRNAs (miR) function as novel diagnostic and prognostic biomarkers and therapeutic targets in Alzheimer’s disease (AD), a common disease among the elderly. In the current study, we aim to explore the effect of miR‐186 on oxidative stress injury of neuron in rat models of AD with the involvement of the interleukin‐2 (IL2) and the Janus kinase/signal transducers and activators of transcription (JAK–STAT) pathways. AD rat models were established, and dual‐luciferase reporter assay and online software were used to confirm the targeting relationship between miR‐186 and IL2. Immunohistochemistry was used evaluating the positive rate of IL2. Afterward, to define the role of miR‐186 in AD, miR‐186, IL2, and JAK–STAT related protein (JAK2, STAT3) expressions were quantified. Cell proliferation was measured by 3‐(4,5‐dimethylthiazol‐2‐yl)2,5‐diphenyl tetrazolium bromide, and cell apoptosis was detected by flow cytometry. We observed downregulated miR‐186 and IL2 and upregulated JAK–STAT signaling pathway related genes in AD. The overexpression of miR‐186 was shown to significantly promote cell proliferation while suppressing cell apoptosis along with the expression of the IL2 and JAK–STAT signaling pathway related protein. Collectively, the key findings obtained from the current study define the potential role of miR‐186 as an inhibitor of AD development by downregulation of IL2 through suppression of the JAK–STAT signaling pathway. - Journal of Cellular Physiology, Volume 233, Issue 12, Page 9488-9502, December 2018.