Abstract
BackgroundNeuroinflammation 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.MethodsThe 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).ResultsThe 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.ConclusionsI/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.
Highlights
Cerebral ischemic injury with high morbidity, disability and mortality worldwide has brought heavy psychological burden and economic pressures to patients and the society [1]
Effects of global cerebral ischemia on cerebral blood flow (CBF) in rats CBF was measured with a moorVMS-LDF laser Doppler blood flow monitor during the operation phase
Our results demonstrated that the time-dependent upregulation of COX2 mRNA and the production of COX2 protein in rat hippocampus persisted for 7 d after ischemia
Summary
Effects of global cerebral ischemia on CBF in rats CBF was measured with a moorVMS-LDF laser Doppler blood flow monitor during the operation phase. SOD activities significantly decreased (P < 0.05) in the early reperfusion periods (2, 6, 24, and 48 h) following global cerebral ischemia, and minimized at 7 d (P < 0.01) compared with the sham-operated group (Figure 1E1). The level of TXB2 significantly decreased at 30 min and 2 h after global ischemia, thereafter began to increase at 6 h (P >0.05) and peaked at 48 h compared to the sham-operated group (Figure 2B). The COX2 in the CA1 significantly increased at 30 min (P < 0.05) and peaked at 7 d (P < 0.01), and thereafter decreased at 15 d, but was still significantly higher compared with the sham-operated group (P < 0.01) (Figure 4B)
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