Evaluation of Sirtuin 1 (SIRT1) and Sirtuin 3 (SIRT3) in serum and cerebrospinal fluid following fatal traumatic brain injury

致命性创伤性脑损伤后血清和脑脊液中Sirtuin 1 (SIRT1) 和Sirtuin 3 (SIRT3) 的评估

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Abstract

Traumatic brain injury (TBI) remains a major contributor to mortality and is frequently the subject of forensic and neuropathological inquiries. In light of ongoing advances in neuroscience and clinical diagnostics, the development of novel bioanalytical methods and data interpretation tools for diagnosing TBI in both living and deceased individuals remains a pressing need. Among the proteins of growing interest are the multifunctional and evolutionarily conserved sirtuin 1 (SIRT1) and sirtuin 3 (SIRT3), due to their adaptive roles in mitochondrial energy metabolism, aging, genomic stability, inflammation, and oncogenesis. This study aimed to determine whether SIRT1 and SIRT3 levels are elevated in post-mortem biofluids, specifically serum and cerebrospinal fluid (CSF) in fatal TBI cases in a population-based autopsy survey. A total of 40 individuals were included, equally divided into two groups, individuals who died from traumatic brain injury (n = 20) and those who died from sudden cardiac or respiratory causes (n = 20), serving as controls. Serum and CSF samples were collected approximately 24 h post-mortem and analyzed using ELISA. The findings demonstrated significantly elevated SIRT1 concentrations in both serum and CSF in the TBI group. Therefore, further analyses demonstrated significantly higher SIRT3 concentrations in serum among study group after TBI. In cases with macroscopically unclear post-mortem abnormalities, a additional assessment of SIRT1 and SIRT3 in body fluids such as serum and CSF might theoretically be utilized to supplementary determination of the cause of death and the magnitude of brain damage for forensic medicine and neuropathological purposes. These findings support the hypothesis that sirtuin expression is altered in the acute phase of TBI and may serve as a useful biomarker in elucidating post-traumatic pathophysiological mechanisms.

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