麦芽醇对大鼠全脑缺血再灌注损伤后海马C-fos表达及神经元凋亡的影响

Effects of Maltol on C-fos Express and Neuron Apoptosis of Cerebral Ischemia-Reperfusion Damages in Rats

目的 研究麦芽醇(MT)对大鼠全脑缺血再灌注损伤的保护作用。方法 Wistar大鼠双侧颈总动脉夹闭30min ,造成全脑缺血,松开动脉夹再灌注。夹闭动脉前后静脉注射1 50 μmol/L麦芽醇生理盐水,动物均于再灌注1h后行C -fos原位杂交,再灌4 8h行TUNEL染色,观察海马神经元的凋亡情况。结果 缺血再灌注后,大鼠海马CA1区C -fos基因表达增强,与对照组相比有统计学意义(P <0 .0 1 )。MT治疗后,C -fos基因表达减弱,与缺血再灌注大鼠比较,C -fos高表达受到明显抑制(P <0 .0 1 ) ;缺血再灌注大鼠的TUNEL染色可见CA1区有大量阳性细胞,MT治疗后,CA1区锥体细胞凋亡值明显减少(P <0 .0 1 )。结论 麦芽醇能使脑缺血导致的C -fos基因表达和细胞凋亡受到抑制,从而减轻海马组织缺血再灌注损伤。

Objective To investigate the protective effect of maltol (MT) on cerebral ischemia-reperfusion damages in rats.Methods Ischemia reperfasion model of Wistar rat was made through removing the clipping.150 μmol/L maltol normal saline was administered by intravenous injection before clipping.The expression of gene C-fos were detected 1 hour and TUNEL staiming was made 48 hours after reperfusion.Results The expression of gene C-fos was increased significantly after ischernio-reperfusion injurg(P<0.01).The enhanced C-fos expression was reduced obviously(P<0.01) after MT treatment.In addition,Many positive cues were observed with TUNEL assay following cerebral ischemia-reperfusion damages.The apoptosis optical density of pyamid cell in CA 1 area reduced obviously after MT treatment(P<0.01).Conclusion Mi can prevent the expression of C-fos and neuronal opoptosis.which induced by cerebral ischemia-reprefusion.MT can prevent C-fos expression and neuronal apoptosis the cerebral ischemia-reperfution induced enhanced,so as to decrease damages in the ischemia-reperfusion injury of hippocampus structure.