中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
21期
9586-9589
,共4页
闫赋琴%滕雅琴%陈充抒%牛玉坚%徐春
閆賦琴%滕雅琴%陳充抒%牛玉堅%徐春
염부금%등아금%진충서%우옥견%서춘
疾病模型,动物%环孢素A%胰岛素%移植后糖尿病
疾病模型,動物%環孢素A%胰島素%移植後糖尿病
질병모형,동물%배포소A%이도소%이식후당뇨병
Disease models,animal%Cyclosporine%Insulin%Post-transplantation diabetes mellitus
目的：建立环孢素A诱发的大鼠糖尿病模型，通过血清胰岛素水平、胰岛素敏感指数、胰岛病理改变探讨环孢素A升高血糖作用的机制。方法雄性SD大鼠20只[（89±10）g]随机等分为两组，每组10只。环孢素A组：环孢素25 mg·kg-1·d-1；对照组：每日给予等量生理盐水，大鼠均在空腹（禁食水8 h）时灌胃给药，用药1 h后喂食。每周测量大鼠体重，每月监测大鼠空腹血糖和环孢素A的血药浓度。用药5个月后于空腹状态下将每组大鼠处死，心脏穿刺取血，4%多聚甲醛体内灌流取胰腺组织，放射免疫方法检测大鼠血清胰岛素水平，胰腺组织行病理组织学观察，应用SPSS 13.0统计软件分析对资料进行统计分析。结果给药4个月后，与环孢素A组平均血糖大于7 mmol/L，说明环孢素A诱发大鼠糖尿病模型成功。与对照组相比，环孢素组大鼠的胰岛素抵抗指数均明显升高（P＜0.05），胰岛素分泌指数明显降低（P＜0.05），环孢素组大鼠胰腺组织的胰导管均遭到破坏，胰岛细胞数量减少，且明显坏死、空泡化。结论环孢素A导致胰岛细胞坏死，减少胰岛素的分泌、增加胰岛素抵抗从而导致大鼠血糖升高。
目的：建立環孢素A誘髮的大鼠糖尿病模型，通過血清胰島素水平、胰島素敏感指數、胰島病理改變探討環孢素A升高血糖作用的機製。方法雄性SD大鼠20隻[（89±10）g]隨機等分為兩組，每組10隻。環孢素A組：環孢素25 mg·kg-1·d-1；對照組：每日給予等量生理鹽水，大鼠均在空腹（禁食水8 h）時灌胃給藥，用藥1 h後餵食。每週測量大鼠體重，每月鑑測大鼠空腹血糖和環孢素A的血藥濃度。用藥5箇月後于空腹狀態下將每組大鼠處死，心髒穿刺取血，4%多聚甲醛體內灌流取胰腺組織，放射免疫方法檢測大鼠血清胰島素水平，胰腺組織行病理組織學觀察，應用SPSS 13.0統計軟件分析對資料進行統計分析。結果給藥4箇月後，與環孢素A組平均血糖大于7 mmol/L，說明環孢素A誘髮大鼠糖尿病模型成功。與對照組相比，環孢素組大鼠的胰島素牴抗指數均明顯升高（P＜0.05），胰島素分泌指數明顯降低（P＜0.05），環孢素組大鼠胰腺組織的胰導管均遭到破壞，胰島細胞數量減少，且明顯壞死、空泡化。結論環孢素A導緻胰島細胞壞死，減少胰島素的分泌、增加胰島素牴抗從而導緻大鼠血糖升高。
목적：건립배포소A유발적대서당뇨병모형，통과혈청이도소수평、이도소민감지수、이도병리개변탐토배포소A승고혈당작용적궤제。방법웅성SD대서20지[（89±10）g]수궤등분위량조，매조10지。배포소A조：배포소25 mg·kg-1·d-1；대조조：매일급여등량생리염수，대서균재공복（금식수8 h）시관위급약，용약1 h후위식。매주측량대서체중，매월감측대서공복혈당화배포소A적혈약농도。용약5개월후우공복상태하장매조대서처사，심장천자취혈，4%다취갑철체내관류취이선조직，방사면역방법검측대서혈청이도소수평，이선조직행병리조직학관찰，응용SPSS 13.0통계연건분석대자료진행통계분석。결과급약4개월후，여배포소A조평균혈당대우7 mmol/L，설명배포소A유발대서당뇨병모형성공。여대조조상비，배포소조대서적이도소저항지수균명현승고（P＜0.05），이도소분비지수명현강저（P＜0.05），배포소조대서이선조직적이도관균조도파배，이도세포수량감소，차명현배사、공포화。결론배포소A도치이도세포배사，감소이도소적분비、증가이도소저항종이도치대서혈당승고。
ObjectiveTo establish cyclosporine A induced diabetes mellitus models in rats and to study the mechanisms of elevating blood glucose by the level of serum insulin, insulin sensitivity index and islet pathological alteration.Methods SD male rats were randomly divided into 2 groups. The rats in cyclosporine group were administrated with cyclosporine 25 mg·kg-1·d-1, while The rats in control group were administrated with equivalent distilled water everyday. Each group were taken intragastric administration on an empty stomach (fasting 8 hours) and were fed after one hour. The weight of rats were measured every week, fasting blood-glucose and blood drug level of CsA were monitored every month. The rats of each group were executed on an empty stomach after 5 months, got blood by cardiac puncture and pancreatic tissue byin vivo perfusion of 4% paraform, the level of serum insulin were tested by radio immunity method, pancreatic tissue were observed in histopathology, and SPSS 13.0 statistical analysis software was used for data analysis.Results The fasting blood glucose levels in cyclosporine group were higher than 7 mmol/L after 4 months, which indicated that cyclosporine induced diabetes mellitus model was established. After 5 months,the insulin resistance index increased significantly(P<0.05), insulin sensitivity index decreased significantly(P<0.05), pancreatic ductal of pancreatic tissues were destroyed, the number of islet cells decreased with necrosis and vacuolization in cyclosporine group than those of control group.Conclusion The hyperglycemic action of cyclosporine is effected by making islet cell necrosis, reducing insulin secretion and increasing insulin resistance.
