CAJ | 학술논문

目的探讨足细胞的数量及nephrin、转化生长因子-β1(TGF-β1)蛋白在阿霉素肾病模型肾小球中的表达及意义.方法建立阿霉素诱导的大鼠肾病模型,于不同实验时间点检测血、尿生化指标;光镜、电镜观察肾脏的组织病理学改变;免疫组化技术检测足细胞数量、nephrin、TGF-β1蛋白的表达情况.结果该模型的肾脏病理学改变明显;1周末足细胞nephrin表达减弱(P<0.05),8周末肾小球TGF-β1表达增强(P<0.05)、足细胞数量减少(P<0.05);nephrin与24h尿蛋白定量(r=-0.83,P<0.01)、尿素氮(r=-0.68,P<0.05)、血肌酐(r=-0.71,P<0.05)呈负相关;TGF-β1与24h尿蛋白定量(r=0.45,P<0.05)、尿素氮(r=0.62,P<0.05)、血肌酐(r=0.59,P<0.05)呈正相关;足细胞数量与24h尿蛋白定量(r=-0.63,P<0.05)、尿素氮(r=-0.72,P<0.05)、血肌酐(r=-0.76,P<0.05)呈负相关;足细胞数量与nephrin呈正相关(r=0.78,P<0.01),与TGF-β1呈负相关(r=-0.64,P<0.05). 结论经改良间隔2周两次尾静脉注射阿霉素(4mg/kg)可以成功复制阿霉素肾病急性和慢性模型;阿霉素肾病蛋白尿的发生和进展与nephrin表达异常密切相关;TGF-β1加重了足细胞数量减少启动的局灶节段性肾小球硬化.
목적 탐토족세포적수량급nephrin、전화생장인자-β1(TGF-β1)단백재아매소신병모형신소구중적표체급의의.방법 건립아매소유도적대서신병모형,우불동실험시간점검측혈、뇨생화지표;광경、전경관찰신장적조직병이학개변;면역조화기술검측족세포수량、nephrin、TGF-β1단백적표체정황.결과 해모형적신장병이학개변명현;1주말족세포nephrin표체감약(P<0.05),8주말신소구TGF-β1표체증강(P<0.05)、족세포수량감소(P<0.05);nephrin여24h뇨단백정량(r=-0.83,P<0.01)、뇨소담(r=-0.68,P<0.05)、혈기항(r=-0.71,P<0.05)정부상관;TGF-β1여24h뇨단백정량(r=0.45,P<0.05)、뇨소담(r=0.62,P<0.05)、혈기항(r=0.59,P<0.05)정정상관;족세포수량여24h뇨단백정량(r=-0.63,P<0.05)、뇨소담(r=-0.72,P<0.05)、혈기항(r=-0.76,P<0.05)정부상관;족세포수량여nephrin정정상관(r=0.78,P<0.01),여TGF-β1정부상관(r=-0.64,P<0.05). 결론경개량간격2주량차미정맥주사아매소(4mg/kg)가이성공복제아매소신병급성화만성모형;아매소신병단백뇨적발생화진전여nephrin표체이상밀절상관;TGF-β1가중료족세포수량감소계동적국조절단성신소구경화.
Objective To investigate podocyte number, the expression of nephrin and transforming growth factor-β1(TGF-β1) in adriamycin-induced-nephropathy rat model and its significance. Methods The rat adriamycin nephrosis model was constructed to detect blood and urine biochemical indicators and observe the pathological changes of renal tissues by light microscope and electron microscope. The expression levels of nephrin and TGF-β1 as well as the podocyte number were examined at different time points by immunohistochemistry. Results The pathological changes of the renal tissues were obvious. Nephrin presented a weak signal at the end of the first week (P<0.05). TGF-β1 started to increase (P<0.05) while the podocyte number started to decrease at the end of the eighth week (P<0.05). Expression of nephrin was negatively correlated with the P<0.05) and serum creatinine (r=-0.71, P<0.05). Expression of TGF-β1 was blood urea nitrogen (r=0.62, P<0.05) and serum creatinine (r=0.59, urinary protein (r=-0.63, P<0.05), blood urea nitrogen (r=-0.72, P<0.05) and serum creatinine (r=-0.76, P<0.05); it was positively correlated with nephrin (r=0.78, P<0.01) but negatively correlated with TGF-β1 (r=-0.64, P<0.05). Conclusion The acute and chronic adriamycin nephrosis models were twice every two weeks. The genesis and development of proteinuria are closely related to the abnormal expression of nephrin. Focal segmental glomerulosclerosis occurs when the podocyte number decreases and TGF-β1 accelerates it.