Cyclooxygenase 2 expression in neonatal rats contributes to hypoxic-ischemic brain damage
Zhang Yu-ping
Abstract
Zhang Yu-ping
Abstract
Objective To study the expression of cyclooxygenase 2 (COX-2) in neonatal rats after hypoxic-ischemic brain damage (HIBD). Methods A model of HIBD in the left brain of 7-day-old Wistar rats was established. The ischemic cortex was sampled for analysis at 2, 6, 24, and 72 h, and 7 d after the onset of hypoxic-ischemic damage. The expression and number of the positive cells of COX-2 in the cortex and hippocampus at different time points were observed by immunohistochemistry. Results Low level of COX-2 immunohistochemical expression was observed in the control group. COX-2 positive cells were upregulated in ischemic brain at 2 h and peaked between 6-24 h significantly (P0.01), but declined at 72 h. Conclusion HIBD can induce the upregulation of COX-2 expression and may participate in hypoxic-ischemic brain injury.
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Objective To study the expression of cyclooxygenase 2 (COX-2) in neonatal rats after hypoxic-ischemic brain damage (HIBD). Methods A model of HIBD in the left brain of 7-day-old Wistar rats was established. The ischemic cortex was sampled for analysis at 2, 6, 24, and 72 h, and 7 d after the onset of hypoxic-ischemic damage. The expression and number of the positive cells of COX-2 in the cortex and hippocampus at different time points were observed by immunohistochemistry. Results Low level of COX-2 immunohistochemical expression was observed in the control group. COX-2 positive cells were upregulated in ischemic brain at 2 h and peaked between 6-24 h significantly (P0.01), but declined at 72 h. Conclusion HIBD can induce the upregulation of COX-2 expression and may participate in hypoxic-ischemic brain injury.
Key concepts: Downregulation and upregulation, Immunohistochemistry, Brain damage, Cyclooxygenase, Hippocampus, Hypoxia (environmental), Cortex (anatomy), Medicine