ArticleArchives of medical science : AMS2026
Vitamin D ameliorated endothelial cell damage induced by diabetes via regulation of lncRNA MEG3 in human umbilical vein endothelial cells.
Article in Archives of medical science : AMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: The purpose of this study was to investigate long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) effects in vitamin D (Vit. D) treatment in endothelial cell damage induced by diabetes. Material and methods: We used human umbilical vein endothelial cells (HUVECs) as a research objective in our study and used high glucose in a diabetic cell model. We evaluated cell apoptosis by flow cytometry, inflammatory factors (IL-6, IL-1β and TNF-α) concentrations by ELISA assay, relative gene and protein expression by RT-qPCR and WB assay, and NF-κB(p65) nuclear volume by cellular immunofluorescence. Results: Compared with the NC (normal control) group, the cell apoptosis rate was significantly increased, inflammatory factor (IL-6, IL-1β and TNF-α) concentrations were significantly up-regulated, lncRNA MEG3 gene expression was significantly depressed, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor κB p65 (NF-κB(p65)) gene and protein expression levels were significantly increased and NF-κB(p65) nuclear volume was significantly up-regulated ( Conclusions: Vit. D improved endothelial cell damage induced by diabetes via lncRNA MEG3 up-regulation
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