标题:Neuronal survival is associated with 72-kDa heat shock protein expression after transient middle cerebral artery occlusion in the rat
作者:Li Y1, Chopp M, Zhang ZG, Zhang RL, Garcia JH.
网址:PMID: 7511157
求助者:fromnow
-
求助时间:2015/6/18 22:41:04
-
求助状态:AB图书馆客服已找到全文,详情咨询在线客服qq 1257749646
-
文献摘要:
Induction of the 72-kDa heat shock protein expression is thought to protect neurons against the subsequent effects of ischemia. However, it is not clear whether the induction of 72-kDa heat shock protein expression by an ischemic event improves neuronal survival. To address this question, we outlined the temporal profile of neuronal induction and expression of the 72-kDa heat shock protein in a model of transient focal ischemia in the rat. Fifty two adult Wistar rats were subjected to middle cerebral artery occlusion of 2 h duration. At 0.5, 3, 6, 9, 12, 24, 48, 96 and 168 h after reopening the artery, coronal brain sections were analyzed using both immunohistochemical methods and hematoxylin and eosin staining to determine the topographic and cellular distribution of the 72-kDa heat shock protein, as well as the extent of neuronal damage. Immunoreactivity to the 72-kDa heat shock protein was not detected in neurons that were destined to become necrotic, and were located in the ischemic core of the brain lesions. However, 72-kDa heat shock protein expression was evident in morphologically intact neurons located in the peripheral zone. The earliest neuronal expression of 72-kDa heat shock protein was detected in animals in which the 2 h occlusion of the middle cerebral artery was followed by 6 h recirculation; the intensity of the 72-kDa heat shock protein immunoreactivity peaked at 48 h, and progressively disappeared 7 days after the ischemic reperfusion event.(ABSTRACT TRUNCATED AT 250 WORDS)
文献《Neuronal survival is associated with 72-kDa heat shock protein expression after transient middle cerebral artery occlusion in the rat》已经找到全文,详情请咨询在线客服 qq 1257749646。
如果您还有其他需要寻找全文的文献,请点击文献求助提交
说明:文献求助是指AB图书馆根据读者的需求,为读者查找论文资料的服务。如果您搜索到相关资料,但不能获取全文,此时便可将有关信息提交求助,由值班客服为您寻找所需文献的全文。提供的文献均来自网络共享资源,不涉及版权交易;如侵犯了您的权利,请告知在线客服,立马删除。文件格式以PDF格式为主。