Serum <scp>miR</scp> ‐598‐3p as a Diagnostic and Prognostic Biomarker for Traumatic Brain Injury: Involvement in Modulating Microglial Inflammation

Traumatic brain injury (TBI) results from external mechanical forces causing brain dysfunction. Dysregulated microRNAs (miRNAs) have been implicated in TBI pathophysiology, but the role of miR-598-3p remains unclear. This study aimed to evaluate the diagnostic and prognostic value of miR-598-3p in TBI and explore its regulatory effects on inflammation in an LPS-induced microglial injury model. Serum miR-598-3p levels were measured via RT-qPCR in 137 TBI patients and 120 controls. ROC curves assessed its diagnostic and prognostic utility. TBI severity was classified by Glasgow Coma Scale (GCS) scores, and outcomes were evaluated using the Glasgow Outcome Scale (GOS). In vitro, LPS-treated BV2 microglia were transfected with a miR-598-3p inhibitor to analyze inflammatory cytokine levels. miR-598-3p expression was significantly elevated in TBI patients versus controls (p < 0.001) and increased progressively with injury severity. ROC analysis demonstrated high diagnostic accuracy for distinguishing TBI severity (AUC = 0.892/0.905) and predicting poor prognosis (AUC = 0.891, sensitivity = 83.33%, specificity = 90.36%). High miR-598-3p expression correlated with elevated Marshall grades, neural injury markers (S100B, GFAP), and pro-inflammatory cytokines (IL-6, TNF-α). Multivariate analysis identified miR-598-3p as an independent risk factor for poor outcomes (OR = 5.03, p < 0.01). miR-598-3p inhibition attenuated LPS-induced IL-6/TNF-α secretion (p < 0.01). Serum miR-598-3p demonstrates clinical utility as a biomarker for TBI diagnosis, severity grading, and prognostic evaluation. Its observed association with amplified microglial inflammatory responses suggests a potential mechanism involving regulation of neuroinflammation pathways.