【摘 要】
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Objective Emerging evidence suggests that limb ischemic preconditioning (LIP) could protect neurons against cerebral ischemia-reperfusion injury.However, the mechanisms of LIP are not well understood.
【机 构】
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Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China
【出 处】
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中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
Objective Emerging evidence suggests that limb ischemic preconditioning (LIP) could protect neurons against cerebral ischemia-reperfusion injury.However, the mechanisms of LIP are not well understood.Neuroglobin (Ngb) is a recently discovered globin that affords protection against hypoxic/ischemic brain injury.The present study is to investigate the neuroprotection of LIP against global cerebral ischemia and its Ngb mechanism.Methods One hundred and thirty-three male Wistar rats were randomly divided into 7 groups: sham of cerebral ischemia group, cerebral ischemia group, LIP+cerebral ischemia group, AS-ODNs+LIP+cerebral ischemia group, S-ODNs+LIP+cerebral ischemia group, hemin+cerebral ischemia group, and hemin vehicle+cerebral ischemia group.Rats in each group were assigned to 3 observations: (1) mitochondrial Na+-K+-ATPase activity at 6 h and 24 h, (2) Bcl-2 and Bax mRNA expression at 24 h, and (3) delayed neuronal death (DND) of pyramidal neurons at 7 d in the CA1 hippocampus.Mitochondrial Na+-K+-ATPase activity was measured using spectrophotometry.The expression of Bcl-2 and Bax mRNA were investigated by reverse transcription-polymerase chain reaction (RT-PCR) method.The DND of pyramidal neurons in the CA1 hippocampus was evaluated by using thionin staining under light microscope by determining the neuronal density and histological grade.Results Pretreatment with LIP or Ngb inducer hemin before cerebral ischemia preserved mitochondrial Na+-K+-ATPase activity and offered protection against cerebral ischemia, whereas administration with Ngb antisense oligodeoxynucleotides (AS-ODNs) inhibited the above effects.Meanwhile, treatment with LIP or hemin prior to cerebral ischemia dramatically up-regulated Bcl-2 mRNA expression, whereas down-regulated Bax mRNA expression.Administration of Ngb AS-ODNs before LIP+cerebral ischemia significantly inhibited Bcl-2 mRNA expression and increased Bax mRNA expression.Conclusion These results indicated that Ngb played an important role in the cerebral ischemic tolerance induced by LIP.
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