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目的:探讨细胞凋亡与肺缺血再灌注损伤的关系以及三七总皂甙的作用及机制。方法:健康日本大耳白兔84只,随机分为对照组、肺缺血再灌注1、3、5h组和三七总皂甙干预1、3和5h组。复制肺缺血再灌注损伤模型。采用原位缺口末端标记(TUNEL)法观测肺组织细胞凋亡指数,免疫组化和原位杂交技术检测肺组织细胞Fas/FasL系统蛋白和基因表达的变化。结果:肺缺血再灌注组肺组织细胞凋亡指数和Fas/FasL蛋白及基因表达均显著高于对照组(均P<0.01)。三七总皂甙干预组Fas/FasLmRNA及其蛋白质的表达显著低于缺血再灌注组(P<0.01),肺组织细胞凋亡指数也显著低于缺血再灌注组(P<0.01)。肺组织细胞凋亡指数分别与Fas/FasL蛋白和Fas/FasLmRNA之间均呈显著正相关(r分别=0.540,0.658,0.668,0.686;均P<0.01)。结论:Fas/FasL系统活化启动的肺组织细胞凋亡可能参与了肺缺血再灌注损伤的发生。三七总皂甙可能通过抑制Fas/FasL系统的激活,阻遏肺组织细胞凋亡,从而减轻肺缺血再灌注损伤。
Objective: To investigate the relationship between apoptosis and lung ischemia-reperfusion injury and the role and mechanism of panax notoginseng saponins. METHODS: Eighty-four Japanese healthy rabbits were randomly divided into control group, lung ischemia-reperfusion group 1, 3, and 5 h groups and panax notoginseng intervention group 1, 3, and 5 h groups. Replicate lung ischemia-reperfusion injury model. The apoptotic index was measured by TUNEL method. The changes of Fas/FasL system protein and gene expression were detected by immunohistochemistry and in situ hybridization. Results: Apoptotic index and Fas/FasL protein and gene expression in lung tissue were significantly higher in lung ischemia-reperfusion group than in the control group (all P<0.01). The mRNA and protein expression of Fas/FasL in the panax notoginseng saponin intervention group was significantly lower than that in the ischemia-reperfusion group (P<0.01), and the apoptotic index in the lung tissue was also significantly lower than that in the ischemia-reperfusion group (P<0.01). The apoptotic index of lung tissue was positively correlated with Fas/FasL protein and Fas/FasL mRNA respectively (r=0.540, 0.658, 0.668, 0.686; all P<0.01). CONCLUSION: Apoptosis of lung tissue activated by Fas/FasL system may be involved in the occurrence of lung ischemia-reperfusion injury. Panax notoginseng saponins may inhibit the apoptosis of lung tissue by inhibiting the activation of Fas/FasL system, thereby reducing lung ischemia-reperfusion injury.