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