Introduction. Diabetes is a chronic inflammatory state, and a key role of lncRNAs in diabetes complications is a new area of research. Methods. In this study, key lncRNAs related to diabetes inflammation were identified by RNA-chip mining and lncRNA-mRNA coexpression network construction and finally verified by RT-qPCR. Results. We ultimately obtained 12 genes, including A1BG-AS1, AC084125.4, RAMP2-AS1, FTX, DBH-AS1, LOXL1-AS1, LINC00893, LINC00894, PVT1, RUSC1-AS1, HCG25, and ATP1B3-AS1. RT-qPCR assays verified that LOXL1-AS1, A1BG-AS1, FTX, PVT1, and HCG25 were upregulated in the HG+LPS-induced THP-1 cells, and LINC00893, LINC00894, RUSC1-AS1, DBH-AS1, and RAMP2-AS1 were downregulated in the HG+LPS-induced THP-1 cells. Conclusions. lncRNAs and mRNAs are extensively linked and form a coexpression network, and lncRNAs may influence the development of type 2 diabetes by regulating the corresponding mRNAs. The ten key genes obtained may become biomarkers of inflammation in type 2 diabetes in the future.

Background The present study mined key lncRNAs and their functions related to inflammation in type 2 diabetes by constructing a lncRNA-mRNA co-expression network based on bioinformatics technology to discover new markers or therapeutic targets. Results We finally obtained 12 genes, including A1BG-AS1, AC084125.4, RAMP2-AS1, FTX, DBH-AS1, LOXL1-AS1, LINC00893, LINC00894, PVT1, RUSC1-AS1, HCG25, and ATP1B3-AS1. RT-qPCR verified that A1BG-AS1, HCG25, and LOXL1-AS1 were upregulated in the HG + LPS-induced THP-1 cell model, and DBH-AS1 was downregulated in the HG + LPS-induced THP-1 cell model. Conclusions LncRNAs and mRNAs are extensively linked and form a co-expression network, and lncRNAs may influence the development of type 2 diabetes by regulating the corresponding mRNAs. The four key genes obtained may become biomarkers of inflammation in type 2 diabetes in the future.

Background Long noncoding RNAs (LncRNAs) have been identified to play an important role in diabetes. The aim of the present study was to determine the expression and function of small nucleolar RNA host gene 16 (SNHG16) in diabetic inflammation. Methods For the in vitro experiments, quantitative real-time PCR (qRT-PCR), Western blotting and immunofluorescence were used to detect LncRNA SNHG16 expression in the high-glucose state. The potential microRNA sponge target of LncRNA SNHG16, miR-212-3p, was detected by dual-luciferase reporter analysis and qRT-PCR. For the in vivo experiments, glucose changes in mice were detected after si-SNHG16 treatment, and SNHG16 and inflammatory factor expression in kidney tissues were detected by qRT-PCR and immunohistochemistry. Results LncRNA SNHG16 was upregulated in diabetic patients, HG-induced THP-1 cells, and diabetic mice. Silencing SNHG16 inhibited the diabetic inflammatory response and the development of diabetic nephropathy. miR-212-3p was found to be directly dependent on LncRNA SNHG16. miR-212-3p could inhibitor P65 phosphorylation in THP-1 cells. The miR-212-3p inhibitor reversed the action of si-SNHG16 in THP-1 cells and induced an inflammatory response in THP-1 cells. LncRNA SNHG16 was also found to be higher in the peripheral blood of diabetic patients than in the normal person. The area under the ROC curve is 0.813. Conclusion These data suggested that silencing LncRNA SNHG16 suppresses diabetic inflammatory responses by competitively binding miR-212-3p to regulate NF-κB. LncRNA SNHG16 can be used as a novel biomarker for patients with type 2 diabetes.