Ataizi, SerdarÖzkoç, MeteKanbak, GüngörKarimkhani, HadiBurukoğlu Dönmez, DilekÜstünışık, NövberÖztürk, Buket10.07.20192019-07-1010.07.20192019-07-102019Ataizi, S., Özkoç, M., Kanbak, G., Karimkhani, H., Dönmez, Dilek B., Üstünışık, N. ... Öztürk, B. (2019). A possible protective role of betain and omega-3 supplementation in traumatic brain injury. Annali Italiani Di Chirurgia, 90(2), 174-181.0003-469X2239-253Xhttps://hdl.handle.net/20.500.12511/1698WOS: 000471139700013PubMed ID: 31182701INTRODUCTION: Due to irreversible damage following head trauma, many overlapping pathophysiological events occur including excitotoxicity, acidotoxicity, ionic imbalance, edema, oxidative stress inflammation and apoptosis. MATERIAL AND METHODS: In this this study, after the rats were separated in to groups theserats were fed throughout fourteen days with betaine, omega-3 or betaine+omega-3 combination in physiological limits prior to the trauma. After a closed head trauma, the damaged brain tissues were collected for biochemically and histologically analyses. This examination involved analyses of levels of caspase-3 and cytochrome C and neuron-specific enolase (NSE) levels in brain tissue. RESULTS: These analyses showed that traumatic brain injury (TBI) caused an increase in the levels of caspase-3, cytochrome C and neuron-specific enolase (NED) in the brain tissues examined. DISCUSSION: In this study, apoptotic and/or necrotic cell death via mitochondrial cytochrome C caspase pathway in traumatized cells and neuron-specific enolase (NED) increase indicative of neuronal damage confirmed the research hypothesis. CONCLUSION: Level of the biomarkers induced by brain injury in the groups fed with betaine, omega-3 and betaine+omega-3 combination before the traumatic damage approximated to that of control group values, suggesting that these products may have a neuroprotective role.eninfo:eu-repo/semantics/openAccessBetainCaspase-3Cytochrome C and Neuron-Specific EnolaseOmega-3Traumatic Brain InjuryArticle902174181Q4Q3