Evaluating the S100β, GFAP, IL-6, and Oxidative Stress Markers in Traumatic Brain Injury

评估创伤性脑损伤中的S100β、GFAP、IL-6和氧化应激标志物

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Abstract

Background Traumatic brain injury (TBI) is a leading cause of neurological morbidity and mortality worldwide. Secondary injury mechanisms such as neuroinflammation and oxidative stress play a pivotal role in the progression of neuronal damage. Biomarkers, including S100β, glial fibrillary acidic protein (GFAP), interleukin-6 (IL-6), and oxidative stress parameters, can reflect the severity and progression of TBI, and their evaluation may assist in clinical decision-making. Objective This study aims to evaluate the serum levels of S100β, GFAP, IL-6, and oxidative stress markers (malondialdehyde (MDA), superoxide dismutase (SOD), and catalase) in patients with TBI compared to healthy controls. Methods This case-control study was conducted at The University of Lahore from July to December 2024. A total of 96 participants were enrolled, including 48 TBI patients and 48 age- and sex-matched healthy controls. Blood samples were collected within 24 hours of injury in TBI patients. Serum concentrations of S100β, GFAP, and IL-6 were measured using ELISA (enzyme-linked immunosorbent assay), while MDA, SOD, and catalase levels were assessed using standard biochemical assays. Data were analyzed using IBM SPSS Statistics for Windows, Version 26 (Released 2019; IBM Corp., Armonk, New York). Independent sample t-tests were used for group comparisons, and Pearson's correlation was applied to examine biomarker relationships. Results TBI patients exhibited significantly higher serum levels of S100β (1.92 ± 0.46 vs. 0.61 ± 0.18 ng/mL), GFAP (3.45 ± 0.71 vs. 1.12 ± 0.33 ng/mL), IL-6 (82.6 ± 18.4 vs. 19.5 ± 7.6 pg/mL), and MDA (5.12 ± 1.03 vs. 2.23 ± 0.66 µmol/L) compared to controls (p < 0.001 for all). SOD and catalase activities were significantly reduced in TBI patients (p < 0.001). S100β and GFAP correlated positively with IL-6 and MDA and negatively with SOD and catalase. Conclusion TBI is associated with elevated neural injury, inflammation, and oxidative stress biomarkers. These findings highlight the diagnostic and prognostic potential of these markers in TBI management.

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