Altered expression of thrombospondin-1/-2 in the cortex and synaptophysin in the hippocampus after middle cerebral artery occlusion and reperfusion

Blood supply returned to infracted tissue causes tissue damage. Therefore, ischemia/reperfusion (I/R) injuries are usually accompanied by synapse formation, but the exact cause is still unknown. To address this question, we established a middle cerebral artery occlusion (MCAO) rat model with different reperfusion times, and we examined neurological deficit scores and brain infarct size. Subsequently, thrombospondin (TSP)-1 and TSP-2 expression levels in the cingulated cortex, striate cortex, aud cortex, and piriform cortex at different time points after I/R were examined using immunohistochemistry (IHC). In addition, synaptophysin expression in the hippocampus was examined using IHC. As expected, after ischemia with different reperfusion times, higher neurological deficits scores were observed in MCAO rats compared to sham-operated rats. Brain infarct sizes were increased in different sections, and brain sections exhibited obvious necrosis in the right cerebra. In addition, TSP-1 and TSP-2 expression levels in the cingulated cortex, striate cortex, aud cortex, and piriform cortex significantly increased with increasing reperfusion times. Similarly, synaptophysin expression levels in the hippocampus significantly increased with increasing reperfusion times. Our results indicate that altered TSP-1 and TSP-2 expression in cortical areas may contribute to synapse formation. Our model not only allowed us to observe the time-related expression of TSP-1, TSP-2, and synaptophysin after I/R injury but also provides a potential tool for studying synapse formation.