| 缺血预处理对再灌注脊髓神经细胞凋亡及细胞凋亡信号调节激酶-1蛋白活化的影响 |
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| 引用本文： | 杨成伟,李丁,殷国勇,刘锋,张宁,蔡卫华,任永信.缺血预处理对再灌注脊髓神经细胞凋亡及细胞凋亡信号调节激酶-1蛋白活化的影响[J].中华创伤骨科杂志,2009,11(1). |
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| 作者姓名： | 杨成伟 李丁 殷国勇 刘锋 张宁 蔡卫华 任永信 |
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| 作者单位： | 1. 浙江省临安市人民医院骨科
2. 南京医科大学第一附属医院骨科,210029 |
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| 基金项目： | 国家自然科学基金，江苏省自然科学基金，江苏省兴卫工程资助项目，江苏省六大人才基金 |
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| 摘 要： | 目的 研究缺血预处理对再灌注脊髓神经细胞凋亡及细胞凋亡信号调节激酶-1(ASKI)蛋白活化的影响.方法 取健康成年新西兰大白兔35只,随机分为空白对照组(5只)、缺血再灌注(1/R)组(15只)、缺血预处理+缺血再灌注(IPC+I/R)组(15只),制作脊髓缺血预处理及缺血再灌注损伤模型.HE染色、电镜检测脊髓神经细胞的形态学变化;Westem-Blot、免疫共沉淀检测ASKl的活化及ASK1-14-3-3相瓦作用的变化.结果 形态学观察:IPC+I/R组脊髓神经细胞凋亡程度、间质出血程度和再灌注相14时段I/R组相比明显减轻.Western.Blot检测ODpASKI/ODASKI定量分析结果显示:空白组为0.142±0.019,I/R组再灌注30 rain、2 h、8 h分别为0.356 4-0.030、0.608±0.029、0.864±0.039,IPC+I/R组再灌注30 min、2 h、8 h分别为0.154±0.029、0.162±0.042、0.462±0.047,IPC+I/R组ASKI活化程度较相同再灌注时段I/R组明显被抑制(P<0.05).免疫共沉淀检测ODASKI/ODl4-3-3定量分析结果显示:空白对照组为0.916±0.058,I/R组再灌注30 min、2 h、8 h分别为0.794±0.040、0.582±0.053、0.270±0.045,IPC+I/R组再灌注30 min、2 h、8 h分别为0.888±0.059、0.830±0.067、0.518±0.043,IPC+I/R组ASKI.14.3.3解离程度较相同再灌注时段I/R组明显被抑制(P<0.05).结论 缺血预处理可减少缺少缺血再灌注损伤过程巾脊髓神经细胞的凋亡,而这种抗凋亡作用可能是通过抑制ASKl-14-3-3的解离进而抑制ASK1的活化来介导的.
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| 关 键 词： | 缺血预处理 再灌注损伤 细胞凋亡 |
Ischemic preconditioning protects the rabbit spinal cord by inhibition of apoptosis induced through the ASK1-dependent pathway during ischemia/reperfusion injury |
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| Abstract: | Objective To investigate the effect of ischemic preconditioning on apoptosis of neuro-cytes and activation of apoptosis signal-regulating kinase 1(ASK1)during ischemia reperfusion injury.Methods Thirty-five New Zealand white rabbits were randomly divided into 3 groups.There were 5 in the sham group, 15 in the ischemia reperfusion(1/R)group, and 15 in the ischemic preconditioning+ischemia reperfusion(IPC+I/R)group.The morphological changes of neurocytes in each group were observed by hema-toxylin and eosin(HE)stain and electron microscopy.The activation of ASK1 and the interaction between ASK1 and 14-3-3 were detected by Western-Blot and immunoprecipitation.Results The apoptosis of neurocytes was significantly less in the IPC+I/R group than in I/R group.The activation of ASK1 and dissociation of ASK1 from 14-3-3 were inhibited in the IPC+I/R group compared with I/R group.Conclusion Ischemic preconditioning may inhibit apoptosis of neurocytes by inhibition of dissociation of ASK1 from 14-3-3 and activation of ASK1 during ischemia reperfusion injury. |
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| Keywords: | Ischemic preconditioning Reperfusion injury Apoptosis |
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