Serum Endocan as a Potential Biomarker in Experimental Subarachnoid Hemorrhage: A Rodent Model Study

Subarachnoid hemorrhage (SAH) is a severe neurological condition in which endothelial dysfunction contributes to early brain injury. However, reliable circulating biomarkers reflecting endothelial activation after SAH remain limited. Endocan, a proteoglycan secreted by activated endothelial cells, has emerged as a potential marker of endothelial dysfunction. This proof-of-concept study aimed to characterize the temporal profile of serum endocan in an experimental SAH model and to explore its association with neuronal injury.

Sixteen male Sprague-Dawley rats were randomly assigned to Sham (n = 8) or SAH (n = 8) groups. SAH was induced by cisterna magna injection of autologous blood. Serum samples were collected at baseline (0), 6, 24, and 48 hours. Endocan concentrations were measured using enzyme-linked immunosorbent assay. Hippocampal neuronal degeneration was assessed histopathologically. Statistical analyses included independent samples t-tests, repeated measures analysis of variance, and Spearman's correlation.

Baseline endocan levels were comparable between groups (P = 0.655). Following SAH induction, serum endocan levels were significantly higher in the SAH group compared with the Sham group at 6 hours (P = 0.023), 24 hours (P < 0.001), and 48 hours (P < 0.001). Within the SAH group, endocan levels increased progressively over time. An exploratory positive correlation was observed between 48-hour endocan levels and hippocampal neuronal degeneration scores (ρ = 0.753, P = 0.031, 95% confidence interval [0.112-0.948]).

In this exploratory experimental study, serum endocan increased over time after SAH and showed an association with neuronal injury severity. These preliminary findings suggest that endocan may reflect endothelial activation during early brain injury after SAH, warranting validation in larger preclinical and clinical studies.