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Updated: Jun 5, 2026
Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
Published on: March 1, 2019
[Study on expression of ELAM-1 and ICAM-1 mRNA on microvascular endothelial cells during focal cerebral
1Department of Clinical Pharmacology, Chinese PLA General Hospital, Beijing 100853, China.
Aim:
To evaluate the role of ELAM-1 and ICAM-1 in the course of inflammatory reactions during focal brain ischemia/reperfusion.
Methods:
The focal brain ischemia/reperfusion model is carried by occluding middle cerebral artery. The expression of ELAM-1 and ICAM-1 mRNA after ischemia/reperfusion was evaluated with RT-PCR.
Results:
No ELAM-1 and ICAM-1 mRNA were detected in the sham-operated cortex and only little in the nonischemic cortex. The expression of ELAM-1 and ICAM-1 mRNA were upregulated at 1 hour, peaked at 6 hour and 3 hour respectively and remained elevated for up to 48 hours after ischemia/reperfusion.
Conclusion:
ELAM-1 and ICAM-1 participate in brain injury during focal ischemia/reperfusion and both of them play an important role in leukocyte infiltration into the ischemic tissues.
Insights
Endothelial-leukocyte adhesion molecule-1 (ELAM-1) and intercellular adhesion molecule-1 (ICAM-1) are upregulated following focal brain ischemia/reperfusion. These molecules play a crucial role in leukocyte infiltration and subsequent brain injury.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Focal brain ischemia/reperfusion triggers inflammatory responses.
- Leukocyte infiltration is a key component of ischemic brain injury.
Purpose of the Study:
- To investigate the role of ELAM-1 and ICAM-1 in focal brain ischemia/reperfusion.
- To assess the expression patterns of ELAM-1 and ICAM-1 mRNA during this process.
Main Methods:
- A focal brain ischemia/reperfusion model was established by occluding the middle cerebral artery.
- Reverse transcription polymerase chain reaction (RT-PCR) was used to quantify ELAM-1 and ICAM-1 mRNA expression.
Main Results:
- ELAM-1 and ICAM-1 mRNA were minimally detected in sham-operated and nonischemic tissues.
- mRNA expression significantly increased by 1 hour post-ischemia, peaking at 6 hours for ELAM-1 and 3 hours for ICAM-1.
- Elevated expression persisted for up to 48 hours after the ischemic event.
Conclusions:
- ELAM-1 and ICAM-1 are integral to the inflammatory cascade in focal brain ischemia/reperfusion.
- Both molecules are critical mediators of leukocyte infiltration into ischemic brain tissue.
- Targeting ELAM-1 and ICAM-1 may offer therapeutic potential for ischemic stroke.
