磷脂酶A_2激活在急性缺血性脑损伤中的作用机制及尼莫地平的保护作用  

Mechanism of phospholipase A_2 and protective effect of nimodipine in acute cerebral ischemic injury

作　　者：王兴勇[1] 李晓文[1] 卢仲毅[1] 匡凤梧[1] 许峰[1] 

机构地区：[1]重庆医科大学儿童医院,400014

出　　处：《中华小儿外科杂志》2004年第4期353-355,共3页Chinese Journal of Pediatric Surgery

基　　金：重庆市科学技术委员会科研基金资助(项目号:2001-54-85)

摘　　要：目的　探讨磷脂酶Ａ2 (ＰＬＡ2 )激活在急性缺血性脑损伤中的作用机制及尼莫地平的保护作。方法　将局灶性脑缺血模型大鼠分为假手术组、缺血组及尼莫地平干预组 ,测定ＰＬＡ2 活力、脑细胞游离Ｃａ2 +浓度、脑含水量及脑组织ＰＬＡ2 表达量的改变。结果　尼莫地平可使缺后脑细胞游离Ｃａ2 +浓度、ＰＬＡ2 活性及脑组织含水量明显降低 ,但对脑缺血后脑组织ＰＬＡ2ｍＲＮＡ表达降低不明显。结论　ＰＬＡ2 激活参与了急性脑损伤的病理过程 ,尼莫地平能抑ＰＬＡ2 活性、降低细胞游离Ｃａ2 +浓度 ,减轻脑水肿的病理改变 ,对缺血性脑细胞损害有一定的保护作用。Objective To investigate the mechanisms of phospholipase A 2(PLA 2) and the protective effect of nimodipine in acute cerebral ischemia injury.Methods Rats was divided into three groups 1)sham operation group, 2) ischemia groups (middle cerebral artery occlusion) and 3) ischemia plus Nimodipine groups. We examined the phospholipase A 2 activity, cytosolic free Ca 2+ concentrations, brain water contents and the expression of sPLA 2 IIA mRNA and the cPLA2 IVmRNA in cerebral cortex 120 minutes after cerebral ischemia.Results The PLA 2 activity, cytosolic free Ca 2+ concentrations in neuronal cells, and brain water contents progressively decreased. The expression of sPLA 2 IIA mRNA and the cPLA 2 IVmRNA in cerebral cortex did not progressively decrease in the Nimodipine group.Conclusions PLA 2 activation is involved in the cerebral ischemia injury. Nimodipine suppresses PLA 2 activity and lowers cytosolic free Ca 2+ concentrations on acute cerebral ischemia injury. It may minimize brain ischaemic damage and swelling.

关 键 词：磷脂酶A2 急性缺血性脑损伤 PLA2 尼莫地平 神经细胞 脑组织 

分 类 号：R741[医药卫生—神经病学与精神病学]