Normobaric oxygen therapy has gained attention as a simple and convenient means of achieving neuroprotection against the pathogenic cascade initiated by acute ischemic stroke.The mechanisms underlying the neuroprotect...Normobaric oxygen therapy has gained attention as a simple and convenient means of achieving neuroprotection against the pathogenic cascade initiated by acute ischemic stroke.The mechanisms underlying the neuroprotective efficacy of normobaric oxygen therapy,however,have not been fully elucidated.It is hypothesized that cerebral hyperglycolysis is involved in the neuroprotection of normobaric oxygen therapy against ischemic stroke.In this study,Sprague-Dawley rats were subjected to either 2-hour middle cerebral artery occlusion followed by 3-or 24-hour reperfusion or to a permanent middle cerebral artery occlusion event.At 2 hours after the onset of ischemia,all rats received either 95%oxygen normobaric oxygen therapy for 3 hours or room air.Compared with room air,normobaric oxygen therapy significantly reduced the infarct volume,neurological deficits,and reactive oxygen species and increased the production of adenosine triphosphate in ischemic rats.These changes were associated with reduced transcriptional and translational levels of the hyperglycolytic enzymes glucose transporter 1 and 3,phosphofructokinase 1,and lactate dehydrogenase.In addition,normobaric oxygen therapy significantly reduced adenosine monophosphate-activated protein kinase mRNA expression and phosphorylated adenosine monophosphate-activated protein kinase protein expression.These findings suggest that normobaric oxygen therapy can reduce hyperglycolysis through modulating the adenosine monophosphate-activated protein kinase signaling pathway and alleviating oxidative injury,thereby exhibiting neuroprotective effects in ischemic stroke.This study was approved by the Institutional Animal Investigation Committee of Capital Medical University(approval No.AEEI-2018-033)on August 13,2018.展开更多
基金partially supported by the National Natural Science Foundation of China,Nos.81802231(to FWL),81871838(to XKG)the Organization Department of Beijing Talents Project,No.2018000082595G485(to FWL)the Science and Technology Plan of Beijing Tongzhou District of China,No.KJ2019CX004(to ZC and FWL).
文摘Normobaric oxygen therapy has gained attention as a simple and convenient means of achieving neuroprotection against the pathogenic cascade initiated by acute ischemic stroke.The mechanisms underlying the neuroprotective efficacy of normobaric oxygen therapy,however,have not been fully elucidated.It is hypothesized that cerebral hyperglycolysis is involved in the neuroprotection of normobaric oxygen therapy against ischemic stroke.In this study,Sprague-Dawley rats were subjected to either 2-hour middle cerebral artery occlusion followed by 3-or 24-hour reperfusion or to a permanent middle cerebral artery occlusion event.At 2 hours after the onset of ischemia,all rats received either 95%oxygen normobaric oxygen therapy for 3 hours or room air.Compared with room air,normobaric oxygen therapy significantly reduced the infarct volume,neurological deficits,and reactive oxygen species and increased the production of adenosine triphosphate in ischemic rats.These changes were associated with reduced transcriptional and translational levels of the hyperglycolytic enzymes glucose transporter 1 and 3,phosphofructokinase 1,and lactate dehydrogenase.In addition,normobaric oxygen therapy significantly reduced adenosine monophosphate-activated protein kinase mRNA expression and phosphorylated adenosine monophosphate-activated protein kinase protein expression.These findings suggest that normobaric oxygen therapy can reduce hyperglycolysis through modulating the adenosine monophosphate-activated protein kinase signaling pathway and alleviating oxidative injury,thereby exhibiting neuroprotective effects in ischemic stroke.This study was approved by the Institutional Animal Investigation Committee of Capital Medical University(approval No.AEEI-2018-033)on August 13,2018.
