SYSTEMIC INFLAMMATORY RESPONSE AND DYSREGULATION OF CARBOHYDRATE METABOLISM FOLLOWING MILD REPETITIVE TRAUMATIC BRAIN INJURY IN RATS
The aim of this study was to comprehensively assess markers of systemic inflammatory response and carbohydrate metabolism in rats following the modeling of mild repetitive traumatic brain injury (mTBI). The experiments were conducted on 28 male Wistar rats weighing 195–220 g, divided into three grou...
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Published in | Актуальні проблеми сучасної медицини Вісник Української медичної стоматологічної академії Vol. 25; no. 2; pp. 141 - 147 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
29.05.2025
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Online Access | Get full text |
ISSN | 2077-1096 2077-1126 2077-1126 |
DOI | 10.31718/2077-1096.25.2.141 |
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Summary: | The aim of this study was to comprehensively assess markers of systemic inflammatory response and carbohydrate metabolism in rats following the modeling of mild repetitive traumatic brain injury (mTBI). The experiments were conducted on 28 male Wistar rats weighing 195–220 g, divided into three groups: Group 1 (control) – intact animals; Group 2 – sham-injured (anesthesia + fixation without trauma, 5 sessions, 48-hour intervals); Group 3 – mTBI modeling (anesthesia, fixation, impact injury, 5 sessions, 48-hour intervals). mTBI was induced by a controlled impact to the skull using a 49.5 g weight under inhalation anesthesia with sevoflurane. On the 14th day after the last exposure, serum levels of neural tissue injury biomarkers, proand anti-inflammatory cytokines, insulin, and glucose were measured. The HOMA-IR index of insulin resistance was calculated. The findings showed that mTBI induces a systemic inflammatory response, evidenced by a significant increase in serum tumor necrosis factor-α and interleukin-6 levels. Elevated S100B protein concentration in the absence of changes in glial fibrillary acidic protein (GFAP) levels indicates subclinical glial cell injury not accompanied by a macrostructural astrocytic reaction. The observed hyperglycemia in rats was primarily due to an insulin-deficient mechanism, as indicated by reduced insulin levels without a further increase in the HOMA-IR index compared to sham-injured animals. The results contribute to a deeper understanding of the pathophysiological mechanisms of mTBI and may serve as a foundation for future research aimed at developing biomarkers and therapeutic strategies for managing traumatic brain injury. |
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ISSN: | 2077-1096 2077-1126 2077-1126 |
DOI: | 10.31718/2077-1096.25.2.141 |