Increased endoplasmic reticulum stress might be related to brain damage in hepatic ischemia-reperfusion injury

Objectives: 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: 12 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), ATF-4 (p=0.001), and EIF2-A (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.