Abstract
Background:
The role of miR-23b-3p in insulin resistance (IR) remained poorly understood.
Methods:
After acacetin injection, obesity-induced IR model was constructed with or without miR-23b-3p upregulation and Neuraminidase 1 (NEU1) overexpression in mice. Body weight, serum metabolite and fat percent of the mice were measured. Tests on oral glucose and insulin tolerance were performed, and inflammatory cytokines C-reactive protein (CRP), Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein 1 (MCP1) levels were quantified with enzyme-linked immunosorbent assay (ELISA). The binding sites between miR-23b-3p and NEU1 were predicted by TargetScan, and verified using dual-luciferase reporter assay. Relative expressions were detected with quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Proportion of Treg and Th17 cells in total CD4+ T cells was detected with flow cytometry.
Results:
MiR-23b-3p offset the effects of acacetin on body weight, fat percent, inflammatory cytokines levels and expressions of markers of regulatory T cells (Treg cells) and T helper 17 cells (Th17 cells), NEU1 and miR-23b-3p. NEU1 was a target of miR-23b-3p, and overexpressed NEU1 reversed the effects of upregulated miR-23b-3p on reducing Treg cells but increased body weight, fat percent and inflammatory cytokines levels, percentage of Th17 cells, and upregulated NEU1 expression.
Conclusion:
Upregulation of miR-23b-3p offset the effects of acacetin on obesity-induced IR through regulating Treg/Th17 cell balance via targeting NEU1.The present findings provide a possible prevention strategy for obesity-induced IR.
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