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Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
Published on: July 31, 2017
Does closure of acid-sensing ion channels reduce ischemia/reperfusion injury in the rat brain?
Jie Wang1, Yinghui Xu1, Zhigang Lian1
1Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China.
Abstract:
Acidosis is a common characteristic of brain damage. Because studies have shown that permeable Ca(2+)-acid-sensing ion channels can mediate the toxic effects of calcium ions, they have become new targets against pain and various intracranial diseases. However, the mechanism associated with expression of these channels remains unclear. This study sought to observe the expression characteristics of permeable Ca(2+)-acid-sensing ion channels during different reperfusion inflows in rats after cerebral ischemia. The rat models were randomly divided into three groups: adaptive ischemia/reperfusion group, one-time ischemia/reperfusion group, and severe cerebral ischemic injury group. Western blot assays and immunofluorescence staining results exhibited that when compared with the one-time ischemia/reperfusion group, acid-sensing ion channel 3 and Bcl-x/l expression decreased in the adaptive ischemia/reperfusion group. Calmodulin expression was lowest in the adaptive ischemia/reperfusion group. Following adaptive reperfusion, common carotid artery flow was close to normal, and the pH value improved. Results verified that adaptive reperfusion following cerebral ischemia can suppress acid-sensing ion channel 3 expression, significantly reduce Ca(2+) influx, inhibit calcium overload, and diminish Ca(2+) toxicity. The effects of adaptive ischemia/reperfusion on suppressing cell apoptosis and relieving brain damage were better than that of one-time ischemia/reperfusion.
Insights
Adaptive reperfusion after cerebral ischemia reduces acid-sensing ion channel 3 expression, lowering calcium influx and toxicity. This approach offers better protection against brain damage and cell apoptosis compared to one-time reperfusion.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Acidosis frequently accompanies brain damage.
- Acid-sensing ion channels (ASICs) mediate calcium ion toxicity, making them therapeutic targets for pain and intracranial diseases.
- Mechanisms regulating ASIC expression in cerebral ischemia remain unclear.
Purpose of the Study:
- To investigate the expression characteristics of permeable Ca(2+)-acid-sensing ion channels during varying reperfusion conditions following cerebral ischemia in a rat model.
- To evaluate the neuroprotective effects of adaptive reperfusion compared to one-time reperfusion.
Main Methods:
- Rat models of cerebral ischemia were subjected to adaptive, one-time, or severe reperfusion.
- Western blot assays and immunofluorescence staining were employed to analyze protein expression.
- Common carotid artery flow and pH levels were monitored.
Main Results:
- Adaptive reperfusion significantly decreased the expression of acid-sensing ion channel 3 and Bcl-x/l compared to one-time reperfusion.
- Calmodulin expression was lowest in the adaptive reperfusion group.
- Adaptive reperfusion restored common carotid artery flow and improved pH, suppressing Ca(2+) influx, calcium overload, and toxicity.
Conclusions:
- Adaptive reperfusion following cerebral ischemia effectively suppresses acid-sensing ion channel 3 expression, mitigating calcium-related neurotoxicity.
- Adaptive reperfusion demonstrates superior neuroprotective effects by reducing cell apoptosis and brain damage compared to one-time reperfusion.
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