title: Does closure of acid-sensing ion channels reduce ischemia/reperfusion injury in the rat brain?
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.
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China.
authors.forename: Yinghui
authors.initials: Y
authors.lastname: Xu
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China.
authors.forename: Zhigang
authors.initials: Z
authors.lastname: Lian
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China.
authors.forename: Tingzhun
authors.initials: T
authors.lastname: Zhu
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China.
authors.forename: Mengkao
authors.initials: M
authors.lastname: Li
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Wei
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China.
authors.forename: Bin
authors.initials: B
authors.lastname: Dong
keywords: acid-sensing ion channel 3; apoptosis; brain injury; calcium overload; calmodulin; cerebral ischemia; grants-supported paper; nerve cells; neural regeneration; neuroregeneration; reperfusion