Limb ischemic preconditioning attenuates apoptosis of pyramidal neurons in the CA1 hippocampus induced by cerebral ischemia-reperfusion in rats.
- Author:
Hong-Gang ZHAO
1
;
Wen-Bin LI
;
Qing-Jun LI
;
Xiao-Ling CHEN
;
Hui-Qing LIU
;
Rong-Fang FENG
;
Jie AI
Author Information
1. Department of Pathophysiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
physiology;
Brain Ischemia;
physiopathology;
Hippocampus;
pathology;
Ischemic Preconditioning;
methods;
Lower Extremity;
blood supply;
Male;
Neurons;
pathology;
Pyramidal Cells;
pathology;
Rats;
Rats, Wistar;
Reperfusion Injury;
prevention & control
- From:
Acta Physiologica Sinica
2004;56(3):407-412
- CountryChina
- Language:English
-
Abstract:
The purpose of this study was to investigate the effects of limb ischemic preconditioning (LIP) on apoptosis of pyramidal neurons in the CA1 hippocampus induced by global cerebral ischemia-reperfusion in rats. Forty-six rats whose bilateral vertebral arteries were occluded permanently were assigned to one of four groups: sham group, limb ischemia group, cerebral ischemia group and LIP group. LIP was performed by occluding the bilateral femoral arteries for 10 min 3 times in an interval of 10 min. Global cerebral ischemia was underwent by occluding the bilateral common carotid arteries for 8 min immediately after LIP. Assays for apoptosis of the hippocampal neurons were biologically and morphologically performed using gel electrophoresis, TUNEL and AO/EB staining. Characteristic DNA ladder was clearly visualized with gel electrophoresis in the hippocampus in cerebral ischemia group, but not in LIP group. The number of TUNEL-positive cells in the CA1 hippocampus was significantly reduced by LIP from 69.8+/-12 (cerebral ischemia group) to 17.8+/-5.8 (P<0.01). AO/EB staining also showed a reduction of apoptosis in LIP group compared with cerebral ischemia group. These results suggest that LIP can inhibit hippocampal neuronal apoptosis induced by cerebral ischemia-reperfusion, which contributes to the protection against the delayed neuronal death induced by cerebral ischemic insult.
