中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2008年
10期
1339-1341,1345
,共4页
维甲酸/药理学%糖尿病%转化生长因子β%肌动蛋白类%肾小管
維甲痠/藥理學%糖尿病%轉化生長因子β%肌動蛋白類%腎小管
유갑산/약이학%당뇨병%전화생장인자β%기동단백류%신소관
Tretinoin/PD%Diabetes mellitus%Transforming growth factor beta%Aetins%Kidney tubules
目的 探讨全反式维甲酸对糖尿病大鼠肾小管一间质转化生长因子β1(TGF-β1)、α平滑肌肌动蛋白(α-SMA)表达的影响.方法 24只链脲佐菌素(STZ)诱导的糖尿病大鼠随机分为治疗组(T),模型组(D)各12只,12只正常组(N),T组给予全反式维甲酸20 ms/(kg·d)油溶液灌胃,D组和N组分别灌等量的植物油.4、8周每组各处死大鼠6只,测量尿微量白蛋白排泄率、肾重/体重、血肌酐(Scr)、血耱.肾组织PAS、Masson染色.免疫组化方法 检测肾小管.问质TGF-β1、α-SMA表达.结果 全反式维甲酸可减轻肾小球系膜区基质、细胞的增生,明显缓解肾小管的损伤,肾间质的基质减少.4周尿微量白蛋白的排泄率实验组低于模型组[(3.08±0.48)μG/min VS(3.35±0.56)μG/min,P<0.05],8周时尿微量白蛋白的排泄率明显低于同期模型组[(2.49±0.40)μg/min Vs(4.53±0.87)μg/min,P<0.01];肾小管-间质TGF-β1、α-SMA表达明显低于模型组(P<0.01).结论 全反式雏甲酸可减轻糖尿病大鼠肾小管.间质的损害,减少尿蛋白.可能通过下调肾小管-间质TGF-β1表达、减少肾小管-间质肌成纤维细胞的数量,防止肾间质的纤维化,保护肾功能.
目的 探討全反式維甲痠對糖尿病大鼠腎小管一間質轉化生長因子β1(TGF-β1)、α平滑肌肌動蛋白(α-SMA)錶達的影響.方法 24隻鏈脲佐菌素(STZ)誘導的糖尿病大鼠隨機分為治療組(T),模型組(D)各12隻,12隻正常組(N),T組給予全反式維甲痠20 ms/(kg·d)油溶液灌胃,D組和N組分彆灌等量的植物油.4、8週每組各處死大鼠6隻,測量尿微量白蛋白排洩率、腎重/體重、血肌酐(Scr)、血耱.腎組織PAS、Masson染色.免疫組化方法 檢測腎小管.問質TGF-β1、α-SMA錶達.結果 全反式維甲痠可減輕腎小毬繫膜區基質、細胞的增生,明顯緩解腎小管的損傷,腎間質的基質減少.4週尿微量白蛋白的排洩率實驗組低于模型組[(3.08±0.48)μG/min VS(3.35±0.56)μG/min,P<0.05],8週時尿微量白蛋白的排洩率明顯低于同期模型組[(2.49±0.40)μg/min Vs(4.53±0.87)μg/min,P<0.01];腎小管-間質TGF-β1、α-SMA錶達明顯低于模型組(P<0.01).結論 全反式雛甲痠可減輕糖尿病大鼠腎小管.間質的損害,減少尿蛋白.可能通過下調腎小管-間質TGF-β1錶達、減少腎小管-間質肌成纖維細胞的數量,防止腎間質的纖維化,保護腎功能.
목적 탐토전반식유갑산대당뇨병대서신소관일간질전화생장인자β1(TGF-β1)、α평활기기동단백(α-SMA)표체적영향.방법 24지련뇨좌균소(STZ)유도적당뇨병대서수궤분위치료조(T),모형조(D)각12지,12지정상조(N),T조급여전반식유갑산20 ms/(kg·d)유용액관위,D조화N조분별관등량적식물유.4、8주매조각처사대서6지,측량뇨미량백단백배설솔、신중/체중、혈기항(Scr)、혈마.신조직PAS、Masson염색.면역조화방법 검측신소관.문질TGF-β1、α-SMA표체.결과 전반식유갑산가감경신소구계막구기질、세포적증생,명현완해신소관적손상,신간질적기질감소.4주뇨미량백단백적배설솔실험조저우모형조[(3.08±0.48)μG/min VS(3.35±0.56)μG/min,P<0.05],8주시뇨미량백단백적배설솔명현저우동기모형조[(2.49±0.40)μg/min Vs(4.53±0.87)μg/min,P<0.01];신소관-간질TGF-β1、α-SMA표체명현저우모형조(P<0.01).결론 전반식추갑산가감경당뇨병대서신소관.간질적손해,감소뇨단백.가능통과하조신소관-간질TGF-β1표체、감소신소관-간질기성섬유세포적수량,방지신간질적섬유화,보호신공능.
Objective To explore the effect of all-trans retinoic acid on the expression of TGF-β1 and ct-SMA of renal tubule-inter-stitium in rats with diabetic nephropathy. Method 24 rats injected with streptozotocin (STZ) were random divided into model (D) and therapy group (T), in addition, 12 normal rats were used as control group (N). The rats in therapy group were administrated with atRA,protein, the ratio of kidney and body weight, serum ereatinine, BS were measured after 4 and 8 weeks. The morphological changes were ob-served by HE, PAS and Masson's staining. The expression of TGF-β1 and αSMA in renal tubule- interstitium were assessed by immunohisto-chemical method. Results atRA reduced proliferation of mesangial cell and matrix, significantly attenuated damage of renal tubule and re-duced extracellular matrix of renal interstitium. Excretory rate of urinary protein in T group was significantly lower after 4 and 8 weeks, com-pared with D group [ ( 3.08±0.48 )μg/min VS ( 3.35±0.56 )μg/min, P<0.05 ; ( 2.49±0.40 )μg/min VS (4.53±0.87 ) μg/min, P<0.01]. The expression of TGF-β1 and αSMA in renal tubule-interstitium were significantly down-regnlated, compared with model group( P<0.01 ). Conclusion atRA alleviated the damage of renal tubule of diabetic nephropathy, reduced urinary protein, prevented fibrosis of renal interstitium by down-regnlation of TGF-β1 expression and reduction of myofibroblast in renal tubule-interstitium.
