Serum miR-197-3p as a diagnostic and prognostic biomarker in traumatic brain injury: involvement in MyD88-dependent microglial polarization.

The prognosis and management of severe traumatic brain injury (TBI) remain significant clinical challenges. The role of serum miR-197-3p in TBI remains unclear. This study aimed to explore its potential as a diagnostic and prognostic biomarker and to elucidate its pathophysiological mechanism. A total of 206 participants were enrolled, including 66 healthy controls, 72 patients with mild-to-moderate TBI, and 68 patients with severe TBI. Serum miR-197-3p expression was measured by qRT-PCR. Its prognostic factors were analyzed via Cox regression models. An oxygen-glucose deprivation (OGD) model was established using the murine microglial BV2 cell line. The regulatory effect of miR-197-3p on microglial polarization was validated by Western blotting and ELISA. Serum levels of miR-197-3p were lowest in patients with severe TBI. The area under the ROC curve for distinguishing severe from mild-to-moderate TBI was 0.872. Low miR-197-3p expression was a potential indicator of poor 6-month functional outcomes in severe TBI patients. miR-197-3p directly targeted the 3'UTR of MyD88 mRNA and inhibited its expression. In the OGD model, overexpression of miR-197-3p suppressed microglial polarization toward the pro-inflammatory (M1) phenotype while promoting a shift toward the anti-inflammatory/reparative (M2) phenotype. This effect was reversed by concurrent overexpression of MyD88. Serum miR-197-3p is a promising candidate biomarker for TBI, showing potential for auxiliary injury severity stratification and as an independent predictor of poor prognosis. Its mechanism may involve modulating neuroinflammation by targeting MyD88 and regulating microglial polarization, warranting further investigation.