摘要
目的观察缺血再灌注后小鼠回肠神经型一氧化氮合酶(neuron alnitric oxide synthase,nNOS)和诱导型一氧化氮合酶(induciblenitric oxide synthase,iNOS)的表达,探讨肠缺血再灌注损伤(ischemia-reperfusion injury,IRI)的发生机制。方法采用小鼠肠系膜上动脉缺血再灌注模型,根据不同再灌注时间对小鼠随机分1d组、3d组、5d组、7d组、对照组和假手术组,用SP法检测小鼠回肠nNOS和iNOS的表达情况。结果与对照组和假手术组相比较,nNOS在再灌注1d后开始在肌间神经丛持续高表达(P<0.01);而iNOS在再灌注3d后开始在肌间神经丛持续高表达(P<0.05)。结论nNOS和iNOS在肠缺血再灌注后的表达增强,提示一氧化氮及一氧化氮合酶与肠神经节细胞在缺血再灌注中的损伤有着密切关系。
Objective To investigate the mechanism of ischemia-reperfusion injury by observing the expression of neuronal nitric oxide synthase （nNOS） and inducible nitric oxide synthase （iNOS） in mouse ileum after ischemia-reperfusion. Methods In a model of superior mesenteric artery occlusion followed by reperfusion in mice, 36 mice were randomly divided into groups according to the time of reperfusion： 1d group, 3d group, 5d group, 7d group, control group and pseudo-operation group. Then, the expression of nNOS and iNOS was observed by immunohistochemical SP method. Results Compared with control group and pseudo-operation group, nNOS showed high immunoreactivity since ld reperfusion following 45 min ischemia （P〈0. 01）, but iNOS kept high immunoreactivity since 3d reperfusion following 45 min ischemia （P〈0.05）. Conclusion The upregulated expression of nNOS and iNOS in mouse ileum after ischemia-reperfusion suggests that NO and NOS are associated with the injury of the intestinal nerve plexus.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2006年第5期542-546,共5页
Chinese Journal of Histochemistry and Cytochemistry
关键词
一氧化氮合酶
一氧化氮
缺血再灌注
回肠
小鼠
Nitric oxide synthase
Nitric oxide
Ischemia-reperfusion
Ileum
Mouse
