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目的:为进一步研究肠外营养(PN)相关肝损害(PNALD)的患病机制及干预措施,建立有效的小鼠模型。方法:将20只小鼠随机分为对照组和模型组,对照组小鼠正常饮食、颈静脉置管后微量泵持续输注等渗盐水;模型组小鼠禁食后颈静脉置管,用微量泵持续输注PN液。1周后比较两组小鼠体重变化,血清生化指标以及肝组织学改变。结果:模型组小鼠体重明显低于对照组(P<0.05),直接胆红素、总胆红素和胆固醇均显著高于对照组(P<0.05),且肝组织在光镜下可见广泛性肝细胞脂肪变性,细胞质内出现大小不一的空泡,主要集中于中央静脉周围。脂肪变性评分为(3.1±0.5)分,显著高于对照组(1.0±0.0)分。结论:模型组小鼠与成人PNALD病人初期的临床和病理改变相似,可用于该病的患病机制,药物治疗疗效以及具体机制的观察和研究。
OBJECTIVE: To establish an effective mouse model to further study the pathogenesis and intervention of parenteral nutrition (PN) -related liver damage (PNALD). Methods: Twenty mice were randomly divided into control group and model group. In the control group, the mice were fed with normal diet. After the jugular vein was cannulated, continuous infusion of isotonic saline was performed by the micro-pump. In the model group, the jugular vein was cannulated after fasting Trace pump continuous infusion of PN liquid. One week later, the weight changes, serum biochemical indexes and liver histological changes of the two groups were compared. Results: The body weight of the model group was significantly lower than that of the control group (P <0.05), and the levels of direct bilirubin, total bilirubin and cholesterol in the model group were significantly higher than those in the control group (P <0.05) Steatosis of hepatic steatosis, vacuoles of varying sizes in the cytoplasm, mainly concentrated around the central vein. Steatosis score was (3.1 ± 0.5) points, significantly higher than the control group (1.0 ± 0.0) points. Conclusion: The initial clinical and pathological changes of PNALD mice in model group are similar to those of PNALD model group, which can be used to study the pathogenesis of the disease, the curative effect of the drug therapy and the specific mechanism.