Molecular mechanism by which mir-153-3p attenuates pulpitis in human deciduous teeth via PTEN-targeted suppression of inflammation and oxidative stress.

This study characterized the expression profile of miR-153-3p in deciduous pulpitis in children, validated its role in regulating inflammation, oxidative stress, and apoptosis via PTEN targeting, and evaluated its biomarker and therapeutic potential. In a prospective design, pulp tissue was collected from 180 children with deciduous-tooth pulpitis (mild, moderate, or severe) and 180 caries-free controls. qRT-PCR was used to quantify miR-153-3p and PTEN expression, VAS pain scores were recorded, and ROC analysis was performed. An LPS-induced inflammatory model (5 µg/mL, 24 h) was established in human dental pulp stem cells, which were transfected with miR-153-3p mimic or PTEN overexpression plasmid. Cell viability, apoptosis, inflammatory cytokines, and oxidative stress markers were subsequently assessed, and correlations among miR-153-3p, VAS, and PTEN were evaluated. miR-153-3p was significantly downregulated in inflamed pulp and inversely correlated with disease severity and VAS score (r = - 0.323, P < 0.001), with an ROC AUC of 0.814. LPS suppressed miR-153-3p and elevated PTEN in a concentration- and time-dependent manner. miR-153-3p upregulation restored viability, reduced apoptosis, decreased cytokine release, increased SOD activity, and lowered MDA content. Dual-luciferase assays confirmed PTEN as a direct target, and PTEN overexpression reversed the protective effects of miR-153-3p. These findings indicate that miR-153-3p downregulation is associated with inflammation severity, and that miR-153-3p attenuates LPS-induced cellular responses by inhibiting PTEN. Its utility in assessing tissue inflammation and potential as a therapeutic target warrant further in vitro and in vivo validation.