Halef Okan Dogan2024-02-272024-02-272023https://hdl.handle.net/20.500.12418/14359Objectives: Our study aimed to investigate the role of endoplasmic reticulum stress (ER) in brain damage following hepatic ischemia-reperfusion (HIR) injury. Specifically, we characterized the expression of markers of ER stress and histopathologic changes in the brain following HIR. Methods: Twelve adults female Wistar rats were divided into two experimental groups equally. Group 1 was designed as the control group, and Group 2 was designed as the HIR group. Blood, liver, and brain tissue samples were collected during the sacrifice. The quantitative ELISA kits were used to detect glucose-regulated protein 78 (GRP-78), activating transcription factor 4 (ATF-4), eukaryotic initiation factor 2 alpha (EIF2-A), caspase-3, caspase-9, and CCAAT/enhancer-binding protein (CEBP) in plasma. Histopathological examination was performed for liver and brain tissues.Results: Higher levels of GRP-78 (p=0.006), ATF4 (p=0.001), and EIF2-Α (p=0.007) were detected in group 2. More damage was detected in liver and brain samples in the histopathological examination of group 2 than in group 1. Conclusions: Our results demonstrate that ER stress is involved in developing brain damage following hepatic ischemia-reperfusion injury, as evidenced by increased expression of markers of ER stress and neuronal injury.en10.1515/tjb-2022-0292info:eu-repo/semantics/openAccessArticle4844394322-s2.0-85173871985N/A1252086WOS:001019056400001Q4