2002•Acta Academiae Medicinae XuzhouRequires access

The mechanisms of NF-κB in brain ischemic injury

Cui Gui

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Abstract

Objective To study the effects of NF-κB in brain ischemic injury by investigating the dynamic rule of NF-κB binding activity in CA1 region of rat hippocampus following global ischemia/reperfusion. Methods Transient cerebral ischemia was induced by 4-vessel occlusion (4-VO). The NF-κB binding activity was determined by EMSA after different periods of reperfusion. The apoptotic condition in the CA1 region after ischemia/reperfusion was studied in paraffin sections by using TUNEL method and electron microscopy. Results The activation of NF-κB in the CA1 region of hippocampus began to increase at 6 h of reperfusion, reached its peak level at 12 h, and began to decline gradually, being at a higher level at 72 h, until the 7d when the activation equaled to that in the sham-operation group. A few apoptotic cells were noticed 24 h after reperfusion (P0.05). The number of them reached the peak level at 72 h (P0.01) and began to decrease after reperfusion for 7 d (P0.05). Conclusion NF-κB is involved in the process of brain ischemia/reperfusion injury, playing varied roles at different phases.

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Objective To study the effects of NF-κB in brain ischemic injury by investigating the dynamic rule of NF-κB binding activity in CA1 region of rat hippocampus following global ischemia/reperfusion. Methods Transient cerebral ischemia was induced by 4-vessel occlusion (4-VO). The NF-κB binding activity was determined by EMSA after different periods of reperfusion. The apoptotic condition in the CA1 region after ischemia/reperfusion was studied in paraffin sections by using TUNEL method and electron microscopy. Results The activation of NF-κB in the CA1 region of hippocampus began to increase at 6 h of reperfusion, reached its peak level at 12 h, and began to decline gradually, being at a higher level at 72 h, until the 7d when the activation equaled to that in the sham-operation group. A few apoptotic cells were noticed 24 h after reperfusion (P0.05). The number of them reached the peak level at 72 h (P0.01) and began to decrease after reperfusion for 7 d (P0.05). Conclusion NF-κB is involved in the process of brain ischemia/reperfusion injury, playing varied roles at different phases.

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Available abstract

Objective To study the effects of NF-κB in brain ischemic injury by investigating the dynamic rule of NF-κB binding activity in CA1 region of rat hippocampus following global ischemia/reperfusion. Methods Transient cerebral ischemia was induced by 4-vessel occlusion (4-VO). The NF-κB binding activity was determined by EMSA after different periods of reperfusion. The apoptotic condition in the CA1 region after ischemia/reperfusion was studied in paraffin sections by using TUNEL method and electron microscopy. Results The activation of NF-κB in the CA1 region of hippocampus began to increase at 6 h of reperfusion, reached its peak level at 12 h, and began to decline gradually, being at a higher level at 72 h, until the 7d when the activation equaled to that in the sham-operation group. A few apoptotic cells were noticed 24 h after reperfusion (P0.05). The number of them reached the peak level at 72 h (P0.01) and began to decrease after reperfusion for 7 d (P0.05). Conclusion NF-κB is involved in the process of brain ischemia/reperfusion injury, playing varied roles at different phases.

Key concepts: Ischemia, TUNEL assay, Reperfusion injury, Apoptosis, Hippocampus, NF-κB, Occlusion, Brain ischemia

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