Akademik Veri Yönetim Sistemi
NEUROGASTROENTEROLOGY AND MOTILITY, cilt.38, sa.2, 2026 (SCI-Expanded, Scopus)
Background Epilepsy is a chronic neurological disorder primarily affecting the central nervous system. However, growing evidence suggests that epilepsy also impacts peripheral organs, including the gastrointestinal tract. The intestinal barrier, essential for maintaining homeostasis and immune defense, is particularly susceptible to oxidative stress, which can disrupt junctional proteins, leading to increased permeability and barrier dysfunction. This study aimed to investigate the effects of epilepsy on duodenal morphology and intercellular junction integrity, as well as to evaluate the potential protective role of Rosa Canina Seed Oil (RSO) in mitigating these alterations. Methods A pilocarpine-induced rat model of epilepsy was employed in 47 male Sprague-Dawley rats, randomly assigned to eight experimental groups, and treated intragastrically with Rosa canina seed oil (RSO) at doses of 0.125, 0.25, or 0.5 mL/rat/day prior to epilepsy induction. Histomorphometric analysis was conducted to assess villus height, crypt depth, and mucosal surface area. Immunohistochemical staining was used to evaluate the expressions of key junctional and cytoskeletal proteins, including zonula occludens-1 (ZO-1), E-cadherin, and vimentin. Correlation analysis was performed to explore associations between morphological parameters and protein expression levels. Results Epileptic rats exhibited significant reductions in villus height, crypt depth, and absorptive surface area, along with downregulation of ZO-1, E-cadherin, and vimentin, indicating compromised barrier function. RSO treatment demonstrated a dose-dependent protective effect, with moderate and high doses partially restoring intestinal morphology and tight junction integrity. Notably, higher doses of RSO significantly restored ZO-1 levels and preserved vimentin expression, suggesting its role in stabilizing the epithelial barrier and cytoskeletal framework. Correlation analysis confirmed a strong association between epilepsy-induced structural disruptions and barrier dysfunction (p < 0.05), highlighting the potential protective effects of RSO. Conclusion These findings demonstrate that epilepsy impairs intestinal barrier integrity by altering epithelial structure and junctional protein expression, leading to increased permeability. RSO treatment partially counteracted these effects, supporting epithelial stability and barrier function in a dose-dependent manner.