This study aimed to investigate the regulatory roles of microRNA-451 (miR-451) on the inflammation and proliferation of glomerular mesangial cells (GMCs) under high-glucose condition, and reveal the potential mechanisms relating with 26S proteasome non-ATPase regulatory subunit 11 (PSMD11) and nuclear factor-kappa B (NF-κB) signaling. The interaction between PSMD11 and miR-451 was identified by dual luciferase reporter gene assay. GMCs were treated with 5.6 mmol/L (normal, L-GMCs) and 30 mmol/L glucose (high-glucose, H-GMCs), respectively. After transfected with pcDNA3.1-PSMD11 and/or miR-451 mimics, the expression of miR-451, PSMD11, inhibitor of NF-κB α (IκBα), phosphorylated IκBα (p-IκBα), NF-κB p65, COX-2, and cyclinD1 were detected in H-GMCs by quantitative real-time PCR and/or western blot. The levels of Interleukin (IL)-1β, IL-6, and IL-8, cell cycle, and viability was detected by enzyme-linked immunosorbent assay, Flow cytometry, and MTT assay, respectively. MiR-451 was upregulated in H-GMCs, and negatively regulated its target PSMD11 (P < 0.05). H-GMCs exhibited significantly higher levels of IL-1β, IL-6, and IL-8, cell viability, and p-IκBα, NF-κB, COX-2 and cyclinD1 expression than L-GMCs (P < 0.05). The transfection of miR-451 mimics significantly decreased the levels of IL-1β, IL-6, and IL-8, inhibited the cell viability via blocking cells in G0/G1 phase, and downregulated p-IκBα, NF-κB p65, COX-2 and cyclinD1 in H-GMCs (P < 0.05). The regulatory effects of miR-451 mimics on H-GMCs were reversed by the transfection of PSMD11 (P < 0.05). The upregulation of miR-451 inhibits the inflammation and proliferation of H-GMCs through downregulating PSMD11 and NF-κB p65.

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