Time course change of COX2-PGI2/TXA2 following global cerebral ischemia reperfusion injury in rat hippocampus
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  • 作者:Lijuan Yu ; Bin Yang ; Jia Wang ; Lei Zhao ; Weinan Luo…
  • 关键词:Global cerebral ischemia reperfusion ; PGI2 ; TXA2 ; COX2 ; PGI2/TXA2 ; Neuroinflammation
  • 刊名:Behavioral and Brain Functions
  • 出版年:2014
  • 出版时间:December 2014
  • 年:2014
  • 卷:10
  • 期:1
  • 全文大小:970 KB
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文摘
Background Neuroinflammation plays pivotal roles in the progression of cerebral ischemia injury. Prostaglandins (PGs) as the major inflammatory mediators in the brain participate in the pathophysiological processes of cerebral ischemia injury. Cyclooxygenase-2 (COX2) is the rate-limiting enzyme of PGs, and thus it is necessary to characterize of the expression patterns of COX2 and its downstream products at the same time in a cerebral ischemia/reperfusion (I/R) model. Methods The levels of prostacyclin (PGI2) and thromboxane (TXA2) and the expression of COX2 were detected in the rat hippocampus at different time points after reperfusion (30?min, 2?h, 6?h, 24?h, 48?h, 7 d, and 15 d). Results The COX2 mRNA and protein expressions in hippocampus both remarkably increased at 30?min, and peaked at 7 d after global cerebral I/R compared with the sham-operated group. The level of PGI2 significantly increased at 2?h after reperfusion, with a peak at 48?h, but was still significantly higher than the sham-operated animals at 15 d. TXA2 level decreased at 30?min and 2?h after reperfusion, but significantly increased at 6?h and peaked at 48?h. PGI2/TXA2 ratio increased at 30?min after reperfusion, and peaked at 48?h compared with the sham-operated animals. Conclusions I/R injury significantly increased the COX2 expression, PGI2 and TXA2 levels, and the PGI2/TXA2 ratio in rat hippocampus in a time-dependent manner. As a consequence, the increased PGI2 level and PGI2/TXA2 ratio may represent a physiological mechanism to protect the brain against the neuronal damage produced by I/R injury.

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