CAJ | 학술논문

目的探索急性肺栓塞(APE)大鼠不规则趋化因子(CX3 CL1)及受体(CX3CR1)的变化及阿司匹林干预作用.方法采用自体血栓法复制APE动物模型,64只大鼠随机分4组:正常组、假手术组、模型组、阿司匹林组.栓塞后4h及72 h检测肺病理,肺组织CX3CL1及CX3CR1的免疫组化.结果栓塞72 h大鼠肺HE染色呈肺泡壁血管高度扩张、充血,个别大鼠光镜下查见出血性梗死灶,应用阿司匹林后肺组织充血程度明显减轻,出现梗死的大鼠数量也有降低的趋势.CX3CL1主要在胞质和胞膜中表达,CX3CR1主要在胞质和核膜中表达,两者在模型组重度阳性表达(++++),阿司匹林轻微阳性表达(+),栓塞后4h及72 h,正常组、假手术组、阿司匹林组的CX3CL1阳性细胞计数均显著小于模型组(P＜0.05)；栓塞后72 h,正常组、假手术组、阿司匹林组的CX3CR1阳性细胞计数均显著小于模型组(10.5±3.5、11.7±5.0、14.6±6.0比20.3 ±5.4,P＜0.05).结论阿司匹林能改善APE大鼠的肺部病理,并抑制APE大鼠肺CX3CL1及CX3CR1的表达.
목적 탐색급성폐전새(APE)대서불규칙추화인자(CX3 CL1)급수체(CX3CR1)적변화급아사필림간예작용.방법 채용자체혈전법복제APE동물모형,64지대서수궤분4조:정상조、가수술조、모형조、아사필림조.전새후4h급72 h검측폐병리,폐조직CX3CL1급CX3CR1적면역조화.결과 전새72 h대서폐HE염색정폐포벽혈관고도확장、충혈,개별대서광경하사견출혈성경사조,응용아사필림후폐조직충혈정도명현감경,출현경사적대서수량야유강저적추세.CX3CL1주요재포질화포막중표체,CX3CR1주요재포질화핵막중표체,량자재모형조중도양성표체(++++),아사필림경미양성표체(+),전새후4h급72 h,정상조、가수술조、아사필림조적CX3CL1양성세포계수균현저소우모형조(P＜0.05)；전새후72 h,정상조、가수술조、아사필림조적CX3CR1양성세포계수균현저소우모형조(10.5±3.5、11.7±5.0、14.6±6.0비20.3 ±5.4,P＜0.05).결론 아사필림능개선APE대서적폐부병리,병억제APE대서폐CX3CL1급CX3CR1적표체.
Objective To explore the intervention of aspirin and the changes of CX3CL1 and its receptor CX3CR1 in a rat model of acute pulmonary embolism (APE).Methods The autologous blood clot method was employed to establish the animal model of APE.A total of 64 rats were randomly divided into 4 groups:normal group (control),sham operation group (sham),model group (model) and aspirin group (aspirin).The profiles of pathology and tissue immunohistochemistry of CX3CL1 and CX3CR1 were compared at 4 h versus 72 h post-embolization.Results At 4 h and 72 h post-embolism,hematoxylin and eosin staining of lung tissue showed a high degree of expansion of alveolar wall vessels and congestion.Furthermore,several rats had hemorrhagic infarction under light microscope.After the dosing of aspirin,hyperemia of lung tissue and the number of rats with infarction significantly decreased.Immunohistochemistry:CX3CL1 was predominantly expressed in cytoplasm and membrane while CX3CR1 in cytoplasm and nuclear membrane.Both showed strongly positive expression in the model group (+ + + +)and slightly positive expression in the aspirin group (+).At 4 h and 72 h post-embolization,the CX3CL1 and CX3CR1-positive cell counts of the control,sham and aspirin groups were significantly less than those of the model group (P ＜ 0.05).Conclusion Aspirin may improve the pathology and inhibit the expression of CX3CL1 and CX3CR1 in APE lung.