Objective To investigate the effects of pergolide on neuronal apoptosis and the expression of apoptotic related gene c-jun in hippocampal CA1 region following forebrain ischemia/ reperfusion(I/R) in gerbils. Methods F...Objective To investigate the effects of pergolide on neuronal apoptosis and the expression of apoptotic related gene c-jun in hippocampal CA1 region following forebrain ischemia/ reperfusion(I/R) in gerbils. Methods Fifty-four gerbils were randomly divided into three groups. Forebrain ischemia was induced by occlusion of bilateral carotid arteries. In sham group, bilateral carotid were dissected and isolated but not occluded. In I/R group, bilateral carotid arteries were dissected and isolated and temporarily clamped for 5 min and then released for reperfusion. In PER group, 1 mg/kg pergolide intraperitoneally injected. HE staining 、TUNEL staining and immunohistochemistry were used to examine the surviving and apoptotic neurons and the expression of c-jun in hippocampal CA1 region at 1 d, 3 d and 7 d after transient ischemia in gerbil. Results 5 min forebrain ischemia resulted in extensive CA1 apoptosis 3 d and 7 d after surgery. About 95% neurons in hippocampal CA1 area entered apoptosis 3 d after reperfusion and only 5% pyramidal neurons stayed surviving 7 d after reperfusion. The expression of c-jun reached its peak at 1 d and disappeared 7 d after reperfusion. Pretreatment of pergolide attenuated neuronal apoptosis and enhanced the number of surviving neurons. Pretreatment of pergolide reduced the expression of c-jun in hippocampal CA1 region. Conclusion Pergolide plays an important role in the protection of hippocampal neurons from apotosis through reducing the expression of c-jun protein.展开更多
文摘Objective To investigate the effects of pergolide on neuronal apoptosis and the expression of apoptotic related gene c-jun in hippocampal CA1 region following forebrain ischemia/ reperfusion(I/R) in gerbils. Methods Fifty-four gerbils were randomly divided into three groups. Forebrain ischemia was induced by occlusion of bilateral carotid arteries. In sham group, bilateral carotid were dissected and isolated but not occluded. In I/R group, bilateral carotid arteries were dissected and isolated and temporarily clamped for 5 min and then released for reperfusion. In PER group, 1 mg/kg pergolide intraperitoneally injected. HE staining 、TUNEL staining and immunohistochemistry were used to examine the surviving and apoptotic neurons and the expression of c-jun in hippocampal CA1 region at 1 d, 3 d and 7 d after transient ischemia in gerbil. Results 5 min forebrain ischemia resulted in extensive CA1 apoptosis 3 d and 7 d after surgery. About 95% neurons in hippocampal CA1 area entered apoptosis 3 d after reperfusion and only 5% pyramidal neurons stayed surviving 7 d after reperfusion. The expression of c-jun reached its peak at 1 d and disappeared 7 d after reperfusion. Pretreatment of pergolide attenuated neuronal apoptosis and enhanced the number of surviving neurons. Pretreatment of pergolide reduced the expression of c-jun in hippocampal CA1 region. Conclusion Pergolide plays an important role in the protection of hippocampal neurons from apotosis through reducing the expression of c-jun protein.
