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Updated: Aug 30, 2026
A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice
Published on: June 22, 2022
Effects of extracellular signal-regulated kinase (ERK) on focal cerebral ischemia
Zhiqiu Wang1, Xiancheng Chen, Liangfu Zhou
1Department of Neurosurgery, Neurological Institute, Huashan Hospital, Fudan University, Shanghai 200040, China. zhiqiuwang@yahoo.com
Objective:
To determine the role of extracellular signal-regulated kinase (ERK)1/2 during focal cerebral ischemia.
Methods:
Left middle cerebral artery occlusion (MCAO) was undergone after the introduction of a nylon suture to the left internal carotid artery in 70 male adult CD-1 mice. ERK 1/2 phosphorylation was detected using Western blot analysis, and the morphological feature was determined by immunohistochemistry. An ERK pathway inhibitor, 1,4-diamino-2,3-dicyano-1,4-bis[2-amino-phenylthio] butadiene (U0126), was administered intravenously 20 minutes before MCAO, and the neurological deficit levels and the infarct volumes were measured 24 hours after MCAO.
Results:
Phosphorylated ERK 1/2 (pERK 1/2) activity increased after 30 minutes of MCAO and peaked at 2 hours. The immunohistochemical study displayed a large number of pERK 1/2 positive cells in the ischemic basal ganglion and surrounding cortex. Double-labeled fluorescent staining identified the pERK1/2 positive cells as neurons or astrocytes. In U0126 treated mice which had undergone 24 hours of MCAO, the neurological deficit levels and the infarct volumes were 44.6% and 45.8% respectively, less than those of the control mice.
Conclusions:
ERK plays an important role in focal cerebral ischemia and inhibition of the ERK pathway can help protect against ischemic brain injury, which may provide a therapeutic approach for cerebral ischemia.
Insights
Extracellular signal-regulated kinase (ERK)1/2 plays a key role in focal cerebral ischemia. Inhibiting the ERK pathway significantly reduced brain injury and neurological deficits in mice, suggesting a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Molecular Biology
- Ischemic Stroke Research
Background:
- Focal cerebral ischemia, a major cause of stroke, involves complex molecular signaling pathways.
- Extracellular signal-regulated kinase (ERK)1/2 is a critical signaling molecule implicated in cellular responses to stress.
Purpose of the Study:
- To elucidate the specific role of extracellular signal-regulated kinase (ERK)1/2 in the context of focal cerebral ischemia.
- To investigate the therapeutic potential of inhibiting the ERK pathway in mitigating ischemic brain damage.
Main Methods:
- Focal cerebral ischemia was induced in mice using middle cerebral artery occlusion (MCAO).
- ERK 1/2 phosphorylation levels were quantified via Western blot analysis.
- The effects of an ERK pathway inhibitor (U0126) on neurological deficits and infarct volume were assessed.
Main Results:
- Phosphorylated ERK 1/2 (pERK 1/2) levels significantly increased in the ischemic brain regions, peaking at 2 hours post-MCAO.
- pERK 1/2 positive cells, identified as neurons and astrocytes, were abundant in the ischemic basal ganglia and cortex.
- Administration of U0126 before MCAO resulted in a substantial reduction (44.6% for neurological deficits, 45.8% for infarct volume) compared to control mice.
Conclusions:
- ERK 1/2 signaling is critically involved in the pathophysiology of focal cerebral ischemia.
- Inhibition of the ERK pathway demonstrates neuroprotective effects, reducing infarct size and neurological impairment.
- Targeting the ERK pathway represents a promising therapeutic avenue for treating ischemic stroke.
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