卡马西平致大鼠消化系统损伤模型的建立

目的：建立卡马西平（CBZ）长期应用致大鼠消化系统损伤的动物模型.方法：SD大鼠72只,随机分为正常对照组（n=12）和模型组（n=60）.正常对照组每d灌胃蒸馏水,其余不做任何处理.模型组大鼠以CBZ灌胃,剂量由600 mg/kg始,每5 d增加200 mg/kg,至1 200 mg/kg维持,共计灌胃120 d,然后停用CBZ,继续观察30d.模型组于给药第30 d、60 d、90 d、120 d及停药30 d后各取大鼠12只测肝功能指标,然后处死大鼠,观察肝、胃和小肠的组织学及超微结构改变.结果：正常对照组状态良好,组织学观察未见异常.模型组大鼠一般情况差,肝细胞弥漫性水肿、点状坏死、炎性细胞浸润;胃黏膜萎缩、组织水肿,炎性细胞浸润,可见浅表溃疡;肝细胞内线粒体和内质网肿胀断裂,线粒体面积增大,密度下降,脂肪滴面积增加;血清AST、ALT、ALP活性升高,ALB含量下降（P＜0.05）.结论：CBZ长期应用致大鼠消化系统损伤模型成功建立.

Establishment of rat digestive system injury model induced by carbamazepine

Aim: To establish a rat digestive system injury model induced by carbamazepine(CBZ). Methods: A total of 72 rats were allocated into 2 groups. Normal control group(n=12) was only given distilled water by gavage and the model group(n=60) was given CBZ from a dose of 600 mg/kg and increased by 200 mg/kg every 5 d till increased to 1 200 mg/kg and maintained the dose till the end of administration.On the 30th d, 60th d, 90th d, 120th d, and 150th d, 12 rats in model group were executed and the hepatic function was assessed and the tissue from the liver, stomach, and small intestines was observed under light microscope and electron transmission microscope. Results: Normal control group was in good condition with normal histological structure; model group was in bad condition with diffuse edema of hepato- cytes, focal necrosis, and inflammatory cell infiltration in liver, gastric mucosa astropy,edema, inflammatory cell infiltration and superficial gastric ulcer as well as endoplasmic reticulum and mitochondrion swelling in hepatocytes and enlarged fat droplet; the serum levels of AST, ALT, and ALP increased and ALB decreased compared with normal control group( P<0.05).Conclusion: The rat digestive system injury model induced by CBZ is successfully established.