医药前沿
醫藥前沿
의약전연
YIAYAO QIANYAN
2014年
11期
92-93
,共2页
肖显杰%梅智强%万卉%杨清%陈慧敏%刘立%方成
肖顯傑%梅智彊%萬卉%楊清%陳慧敏%劉立%方成
초현걸%매지강%만훼%양청%진혜민%류립%방성
慢性移植肾病%自身免疫%病理
慢性移植腎病%自身免疫%病理
만성이식신병%자신면역%병리
chronic%allograft nephropathy%autoimmunity%pathology
目的:测量与评估大鼠慢性移植肾病中自身免疫反应的致病强度。方法:使用F344、Lewis大鼠分别为供受体建立经典慢性移植肾肾病模型(CAN组)。改良CAN模型保留受体一侧自体健肾建立自体肾损害观测模型(AI组)。使用正常Lewis大鼠建立肾单纯缺血再灌注模型(IR组)。以Lewis大鼠肾缺血再灌注并同系CAN大鼠脾细胞过继模型为AR组。以Lewis大鼠自体肾移植作为对照(Syn组)。动态监测各组模型生存曲线、蛋白尿水平动态变化。40周检测自体肾肾小球硬化指数(GSI)。结果:CAN组蛋白尿水平在肾移植后第6周开始上升,第32周上升至(1.72±0.06) g/mmol。其存活率第57天为85.7%,第94天为42.9%,至260天为0。AI和IR组蛋白尿水平至40周维持正常(<0.05g/mmol)。而AR组在第18周出现蛋白尿水平异常(0.18±0.03)g/mmol,其后持续缓慢上升至40周为(0.23±0.04)g/mmol。该组第97天存活率为80%保持至第280天。第40周检查AR组自体肾GSI为(1.24±0.16)。结论:大鼠肾移植继发自身免疫40周致肾功能轻度异常,但肾小球硬化面积已达25%。
目的:測量與評估大鼠慢性移植腎病中自身免疫反應的緻病彊度。方法:使用F344、Lewis大鼠分彆為供受體建立經典慢性移植腎腎病模型(CAN組)。改良CAN模型保留受體一側自體健腎建立自體腎損害觀測模型(AI組)。使用正常Lewis大鼠建立腎單純缺血再灌註模型(IR組)。以Lewis大鼠腎缺血再灌註併同繫CAN大鼠脾細胞過繼模型為AR組。以Lewis大鼠自體腎移植作為對照(Syn組)。動態鑑測各組模型生存麯線、蛋白尿水平動態變化。40週檢測自體腎腎小毬硬化指數(GSI)。結果:CAN組蛋白尿水平在腎移植後第6週開始上升,第32週上升至(1.72±0.06) g/mmol。其存活率第57天為85.7%,第94天為42.9%,至260天為0。AI和IR組蛋白尿水平至40週維持正常(<0.05g/mmol)。而AR組在第18週齣現蛋白尿水平異常(0.18±0.03)g/mmol,其後持續緩慢上升至40週為(0.23±0.04)g/mmol。該組第97天存活率為80%保持至第280天。第40週檢查AR組自體腎GSI為(1.24±0.16)。結論:大鼠腎移植繼髮自身免疫40週緻腎功能輕度異常,但腎小毬硬化麵積已達25%。
목적:측량여평고대서만성이식신병중자신면역반응적치병강도。방법:사용F344、Lewis대서분별위공수체건립경전만성이식신신병모형(CAN조)。개량CAN모형보류수체일측자체건신건립자체신손해관측모형(AI조)。사용정상Lewis대서건립신단순결혈재관주모형(IR조)。이Lewis대서신결혈재관주병동계CAN대서비세포과계모형위AR조。이Lewis대서자체신이식작위대조(Syn조)。동태감측각조모형생존곡선、단백뇨수평동태변화。40주검측자체신신소구경화지수(GSI)。결과:CAN조단백뇨수평재신이식후제6주개시상승,제32주상승지(1.72±0.06) g/mmol。기존활솔제57천위85.7%,제94천위42.9%,지260천위0。AI화IR조단백뇨수평지40주유지정상(<0.05g/mmol)。이AR조재제18주출현단백뇨수평이상(0.18±0.03)g/mmol,기후지속완만상승지40주위(0.23±0.04)g/mmol。해조제97천존활솔위80%보지지제280천。제40주검사AR조자체신GSI위(1.24±0.16)。결론:대서신이식계발자신면역40주치신공능경도이상,단신소구경화면적이체25%。
Objective: To measure and evaluate the pathogenic strength of autoimmune reaction in chronic renal al ograft nephropathy of rats. Methods: Lewis recipients with a F344 al ograft was set up as the classic chronic al ograft nephropathy model (CAN group). Improved CAN model which the receptors retain other side of autologous kidney served as autologous renal damages model (AI group). Renal ischemia-reperfusion model (IR group) was established using normal rats. Lewis rats with renal ischemia-reperfusion and adoption of splenocytes from syngenic CAN rats served as AR group. Syngenic renal transplants acted as the controls (Syn group). Dynamic monitored the survival curve and proteinuria changes of al models and Detected autologous renal glomerulosclerosis index (GSI) in 40w. Results: After 6 weeks the proteinuria of CAN group began increasing and then developed that reach (1.72±0.06) g/mmol at the 32th week, whose survival rate was 85.7% in the 57th day, 42.9% in the 94th day, and zero in the 260th day. The proteinuria of group AI and IR had maintained the normal level (<0.05g/mmol) to the 40th week. After 18 weeks the proteinuria of group AR began increasing to (0.18±0.03) g/mmol and then developed slowly that reach (0.23±0.04) g/mmol at the 40th week. Its survival rate was 80% in the 97th day and held onto the 280th day. The autologous renal GSI of AR group was (1.24±0.16) detected in 40th week. Conclusion: Subsequent autoimmunity fol owing renal transplantation in rats caused mild abnormality of renal functional in 40 weeks but the ratio of glomerular sclerosis area could reach 25%.