Protective effects of miRNA-589 on cerebral ischemia-reperfusion injury

G. P. Ma; B. Z. Yang; Y. S. Zhang; B. Wang; X. H. Wei; R. F. Zhang; K. H. Jia; J. P. Gao

doi:10.23812/20-52-A

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Asia Pacific Academy of Science Pte. Ltd. (APACSCI) specializes in international journal publishing. APACSCI adopts the open access publishing model and provides an important communication bridge for academic groups whose interest fields include engineering, technology, medicine, computer, mathematics, agriculture and forestry, and environment.

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Macrophages in the pathogenesis of psoriasis and anti-psoriatic nanotherapies

Psoriasis is a common, chronic, and inflammatory skin disease. Macrophages account for about 61.3% of the inflammatory cells infiltrating psoriatic lesions. Modulating macrophage polarization, inhibiting their infiltration, and targeting the secretion of inflammatory factors and associated inflammatory pathways by these cells can alleviate psoriasis symptoms and inflammation. Moreover, nanomaterials as novel drug carriers, offer unique advantages such as large surface area, easy modification, high biocompatibility, good biodegradability, enhanced systemic adsorption, etc. Nanomaterials have great potential for efficient drug delivery and release, as well as improving therapeutic efficacy while reducing adverse effects. By systematically addressing the role of macrophages in psoriasis pathogenesis and the potential of nanomaterials in treating psoriasis through modulating macrophages, this review enhances our understanding of the disease mechanism and holds promise for novel therapeutic breakthroughs and advancements in the future treatment of psoriasis.

Protective effects of miRNA-589 on cerebral ischemia-reperfusion injury

G. P. Ma, B. Z. Yang, Y. S. Zhang, B. Wang, X. H. Wei, R. F. Zhang, K. H. Jia, J. P. Gao

Article ID: 4807
Vol 34, Issue 4, 2020

DOI: https://doi.org/10.23812/20-52-A

Received: 8 September 2020; Accepted: 8 September 2020; Available online: 8 September 2020; Issue release: 8 September 2020

Abstract

To uncover the potential influence of microRNA-589 (miRNA-589) on cerebral ischemia-reperfusion injury (IRI) and the underlying mechanism, BV2 cells were stimulated by lipopolysaccharide (LPS) or conditioned medium (CM) of primary cortical neurons undergoing oxygen-glucose deprivation (OGD). Regulatory effects of miRNA-589 on the release of inflammatory factors in BV2 cells induced with LPS or CM of primary cortical neurons undergoing OGD were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). The interaction between miRNA-589 and TRAF6 was finally assessed by dual-luciferase reporter gene assay. MiRNA-589 was downregulated in BV2 cells induced with LPS or CM of primary cortical neurons undergoing OGD. Overexpression of miRNA-589 reduced the release of inflammatory factors in LPS or CM-induced BV2 cells. TRAF6 was verified to be the downstream gene of miRNA-589, and its level was negatively regulated by miRNA-589. MiRNA-589 is downregulated following cerebral IRI and alleviates inflammatory response through negatively regulating TRAF6.

Keywords

BV2;MiRNA-589;TRAF6;cerebral IRI;inflammation

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Medical Genetics, University of Torino Medical School, Italy

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