Neurological research · 2026
Serum endocan as a circulating biomarker following experimental spinal cord injury in rats.
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Kullukçu Hümeyra, Cetinkaya Kadir, Özgür Özates Mehmet, Ünsal Yasar, Gürcan Oktay, Kazancı Atilla, Önder Evrim, Saadet Deveci Bulut Tuba, Gürhan Gürcay Ahmet
Аннотация
BACKGROUND: Spinal cord injury (SCI) is a severe neurological disorder causing long-term disability and socioeconomic burden. Secondary injury mechanisms, including inflammation, ischemia, and endothelial dysfunction, contribute to progressive tissue damage. The identification of reliable circulating biomarkers associated with these pathological processes remains a critical area of research.
OBJECTIVE: This study investigated temporal changes in serum endothelial cell-specific molecule-1 (endocan) in an experimental SCI model and its potential association with early histopathological changes following injury.
METHODS: Sixteen adult male Sprague - Dawley rats were randomly assigned to laminectomy-only (L, n = 8) or laminectomy plus trauma (LT, n = 8). SCI was induced at L4-L5 using a modified Allen weight-drop technique. Serum endocan was measured at baseline (immediately prior to trauma induction) and 6, 24, and 48 hours post-injury via enzyme-linked immunosorbent assay. Histopathology of hematoxylin and eosin - stained sections assessed neuronal degeneration semi-quantitatively. Temporal changes and correlations were analyzed.
RESULTS: Serum endocan increased over time in both groups, with higher levels in the trauma group at 24 and 48 hours (p < 0.05). No difference was seen at 6 hours. Histopathology showed greater neuronal degeneration in the trauma group (p = 0.001). Endocan levels correlated positively with degeneration scores (r = 0.809, p < 0.05).
CONCLUSIONS: Serum endocan rises after experimental SCI and correlates with histopathological severity, suggesting its potential as a biomarker of endothelial dysfunction in secondary injury. Further studies are needed to evaluate prognostic value.
OBJECTIVE: This study investigated temporal changes in serum endothelial cell-specific molecule-1 (endocan) in an experimental SCI model and its potential association with early histopathological changes following injury.
METHODS: Sixteen adult male Sprague - Dawley rats were randomly assigned to laminectomy-only (L, n = 8) or laminectomy plus trauma (LT, n = 8). SCI was induced at L4-L5 using a modified Allen weight-drop technique. Serum endocan was measured at baseline (immediately prior to trauma induction) and 6, 24, and 48 hours post-injury via enzyme-linked immunosorbent assay. Histopathology of hematoxylin and eosin - stained sections assessed neuronal degeneration semi-quantitatively. Temporal changes and correlations were analyzed.
RESULTS: Serum endocan increased over time in both groups, with higher levels in the trauma group at 24 and 48 hours (p < 0.05). No difference was seen at 6 hours. Histopathology showed greater neuronal degeneration in the trauma group (p = 0.001). Endocan levels correlated positively with degeneration scores (r = 0.809, p < 0.05).
CONCLUSIONS: Serum endocan rises after experimental SCI and correlates with histopathological severity, suggesting its potential as a biomarker of endothelial dysfunction in secondary injury. Further studies are needed to evaluate prognostic value.