Related Experiment Video
Updated: Apr 19, 2026
2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
[Changes of endoplasmic reticulum stress- and apoptosis-related factors in rat cerebral cortex following controlled
Jianxing Zhang1, Hongying Li, Guobin Zhou
1Department of Anesthesiology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China.E-mail: jianxingzhang_edu@163.com.
Objective:
To investigate the changes of endoplasmic reticulum stress (ERS)- and apoptosis-related factors in rat cerebral cortex following controlled hypotension.
Methods:
Twenty-four healthy male SD rats were randomly divided into 4 equal groups, including a sham hypotension group (group A) and 3 hypotension groups with the mean arterial pressure maintained for 60 min at 70 mmHg (group B), 50 mmHg (group) and 30 mmHg (group D) with sodium nitroprusside and esmolol. All the rats received an equal volume of fluid infusion. Twelve hours after controlled hypotension, the rats were sacrificed to examine the protein expressions of Bax, Bcl-2, glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and caspase-12 in the cortex with Western blotting. GRP78 mRNA expression was measured by RT-PCR, and the cell apoptosis was evaluated by TUNEL staining.
Results:
Compared with those in group A, GRP78 mRNA and protein expressions of GRP78, CHOP, caspase-12 related with ERS increased significantly in groups C and D (P<0.05), especially in group D (P<0.05), but not in group B (P>0.05). Apoptotic cells and Bax expression increased and Bcl-2 expression decreased significantly in groups C and D (P<0.05), but not in group B (P>0.05); such changes were more prominent in group D than in group C (P<0.05).
Conclusion:
Mild controlled hypotension (70 mmHg) does not induce neuronal injury in rat cerebral cortex, but severe hypertension (lower than 50 mmHg) can cause neuronal ERS and apoptosis.
