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Updated: May 18, 2026

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
Published on: March 1, 2019
E-selectin deficiency attenuates brain ischemia in mice.
Xiu-Juan Ma1, Jin-Wei Cheng, Jing Zhang
1Department of Pharmacology, College of Pharmacy, Second Military Medical University, Shanghai, China.
E-selectin deficiency protects against brain ischemia by reducing inflammation and apoptosis. This finding offers a potential therapeutic target for stroke treatment.
Area of Science:
- Neuroscience
- Immunology
- Cardiovascular Research
Background:
- E-selectin plays a role in inflammatory responses.
- Cerebral ischemia, a major cause of stroke, involves complex inflammatory processes.
Purpose of the Study:
- To investigate the protective effect of E-selectin deficiency in a mouse model of focal cerebral ischemia.
- To explore the underlying mechanisms involving inflammation and apoptosis.
Main Methods:
- E-selectin levels were assessed in rat models.
- E-selectin knockout (Es(-/-)) and wild-type (WT) mice underwent middle cerebral artery occlusion (MCAO).
- Neurological function, infarct size, inflammatory markers (MPO, IL-1β, TNF-α), and apoptosis were evaluated.
Main Results:
- E-selectin deficiency improved neurological function and reduced infarct area after MCAO.
- Lower levels of MPO and IL-1β were observed in Es(-/-) mice compared to WT mice.
- Apoptosis was significantly reduced in Es(-/-) mice post-MCAO.
Conclusions:
- E-selectin deficiency demonstrates a protective effect against cerebral ischemia.
- This protection is attributed to the inhibition of inflammation and apoptosis.
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