Hui Zhang, Benjuan Liang, Yu Chang, Zhen Zhang, Zheng Wang, Wenwen Zhu, Bing Song, Haoqiang Zhang
BackgroundNeuroinflammation has been implicated in diabetic cognitive dysfunction, with the NLRP3 playing an important role.ObjectiveThis study aimed to elucidate the regulatory role of miR-223-3p in NLRP3 associated neuroinflammation and its potential as a biomarker for mild cognitive impairment (MCI) in type 2 diabetes mellitus (T2DM).MethodsDiabetic mouse models were generated by 24 weeks of high-fat diet feeding, with cognitive impairment verified by behavioral assessments. Hippocampal tissues were analyzed by microRNA sequencing and validated for miR-223-3p expression. NLRP3-mediated neuroinflammation was examined in vivo, while in vitro assays using BV2 cells assessed mechanistic pathways. BV2 cells with miR-223-3p knockdown and overexpression to evaluate its effects on NLRP3. Clinically, plasma exosomal miR-223-3p was quantified in T2DM patients with and without MCI and correlated with neuropsychological test scores.ResultsDiabetic mice exhibited cognitive decline, reduced hippocampal miR-223-3p, microglial activation, and elevated NLRP3 and pro-inflammatory cytokines. miR-223-3p knockdown and overexpression induced and attenuated neuroinflammation, respectively. Luciferase reporter gene assays confirmed the direct regulatory of miR-223-3p on NLRP3. Clinically, exosomal miR-223-3p levels were significantly lower in T2DM patients with MCI (n = 98) compared with cognitive normal patients (n = 147), correlating with global cognition, and immediate memory performance. ROC analysis demonstrated that, when using the threshold of 0.7565, miR-223-3p achieved a diagnostic specificity of 71.4% and a sensitivity of 68.7% for identifying MCI.ConclusionsmiR-223-3p exerts neuroprotective effects by suppressing NLRP3-mediated neuroinflammation. Its downregulation contributes to cognitive impairment in diabetes, and circulating exosomal miR-223-3p represents a potential biomarker for identifying MCI in T2DM.