中华糖尿病杂志
中華糖尿病雜誌
중화당뇨병잡지
CHINES JOURNAL OF DLABETES MELLITUS
2010年
3期
200-204
,共5页
糖尿病肾病%色素上皮衍生因子%转化生长因子-β1%罗格列酮
糖尿病腎病%色素上皮衍生因子%轉化生長因子-β1%囉格列酮
당뇨병신병%색소상피연생인자%전화생장인자-β1%라격렬동
Diabetic nephropathy%Pigment epithelium-derived factor%Transforming growth factor-β1%Rosiglitazone
目的 观察罗格列酮对糖尿病大鼠肾脏色素上皮衍生因子和转化生长因子-β1蛋白表达的影响.方法 健康雄性SD大鼠42只(体重180～200 g),采用随机数字表法分为正常对照组(n=14)、糖尿病组(n=14)和罗格列酮干预组(n=14).腹腔注射链脲佐菌素,建立糖尿病大鼠模型.造模成功后,罗格列酮干预组给予罗格列酮5μ·g-1·d-1灌胃治疗12周,正常对照组注射等体积柠檬酸缓冲液.12周末检测各组大鼠血糖、血脂、肝功能、肾脏指数、肾功能、24h尿白蛋白排泄率及血清色素上皮衍生因子含量.采用HE染色观察大鼠肾脏组织形态学变化,应用免疫组织化学法和Western blot检测肾脏色素上皮衍生因子和转化生长因子-β1蛋白表达水平.运用t检验和方差分析进行数据统计.结果 与正常对照组比较,糖尿病组大鼠肾小球肥大,基底膜增厚,系膜区基质明显增生,部分肾小管呈空泡变性,转化生长因子-β1蛋白表达水平明显升高(免疫组织化学分析:4.60 ±0.14、1.57±0.14,t=3.052,P<0.01;Western blot:1053±64、462±70,t=2.817,P<0.01),而色素上皮衍生因子蛋白表达水平显著降低(免疫组织化学分析:1.53±0.12、3.96±0.18,t=2.845,P<0.01:Western blot:228±275、698±120,t=3.152,P<0.01).与糖尿病组比较,罗格列酮干预组大鼠肾小球肥大,基底膜增厚,系膜区基质增生程度明显减轻,转化生长因子-β1蛋白表达水平明显降低(免疫组织化学分析:2.79±0.16、4.60±0.14,t=2.964,P<0.01;Western blot:753±81、1053±64,t=2.884,P<0.01),色素上皮衍生因子蛋白表达水平显著升高(免疫组织化学分析:2.64±0.32、1.53±0.12,t=2.347,P<0.05;Western blot:473±127、228±275,t=2.334,P<0.05).结论 罗格列酮可通过下调糖尿病大鼠肾脏转化生长因子-β1蛋白表达、上调色素上皮衍生因子蛋白表达来发挥肾脏保护作用.
目的 觀察囉格列酮對糖尿病大鼠腎髒色素上皮衍生因子和轉化生長因子-β1蛋白錶達的影響.方法 健康雄性SD大鼠42隻(體重180～200 g),採用隨機數字錶法分為正常對照組(n=14)、糖尿病組(n=14)和囉格列酮榦預組(n=14).腹腔註射鏈脲佐菌素,建立糖尿病大鼠模型.造模成功後,囉格列酮榦預組給予囉格列酮5μ·g-1·d-1灌胃治療12週,正常對照組註射等體積檸檬痠緩遲液.12週末檢測各組大鼠血糖、血脂、肝功能、腎髒指數、腎功能、24h尿白蛋白排洩率及血清色素上皮衍生因子含量.採用HE染色觀察大鼠腎髒組織形態學變化,應用免疫組織化學法和Western blot檢測腎髒色素上皮衍生因子和轉化生長因子-β1蛋白錶達水平.運用t檢驗和方差分析進行數據統計.結果 與正常對照組比較,糖尿病組大鼠腎小毬肥大,基底膜增厚,繫膜區基質明顯增生,部分腎小管呈空泡變性,轉化生長因子-β1蛋白錶達水平明顯升高(免疫組織化學分析:4.60 ±0.14、1.57±0.14,t=3.052,P<0.01;Western blot:1053±64、462±70,t=2.817,P<0.01),而色素上皮衍生因子蛋白錶達水平顯著降低(免疫組織化學分析:1.53±0.12、3.96±0.18,t=2.845,P<0.01:Western blot:228±275、698±120,t=3.152,P<0.01).與糖尿病組比較,囉格列酮榦預組大鼠腎小毬肥大,基底膜增厚,繫膜區基質增生程度明顯減輕,轉化生長因子-β1蛋白錶達水平明顯降低(免疫組織化學分析:2.79±0.16、4.60±0.14,t=2.964,P<0.01;Western blot:753±81、1053±64,t=2.884,P<0.01),色素上皮衍生因子蛋白錶達水平顯著升高(免疫組織化學分析:2.64±0.32、1.53±0.12,t=2.347,P<0.05;Western blot:473±127、228±275,t=2.334,P<0.05).結論 囉格列酮可通過下調糖尿病大鼠腎髒轉化生長因子-β1蛋白錶達、上調色素上皮衍生因子蛋白錶達來髮揮腎髒保護作用.
목적 관찰라격렬동대당뇨병대서신장색소상피연생인자화전화생장인자-β1단백표체적영향.방법 건강웅성SD대서42지(체중180～200 g),채용수궤수자표법분위정상대조조(n=14)、당뇨병조(n=14)화라격렬동간예조(n=14).복강주사련뇨좌균소,건립당뇨병대서모형.조모성공후,라격렬동간예조급여라격렬동5μ·g-1·d-1관위치료12주,정상대조조주사등체적저몽산완충액.12주말검측각조대서혈당、혈지、간공능、신장지수、신공능、24h뇨백단백배설솔급혈청색소상피연생인자함량.채용HE염색관찰대서신장조직형태학변화,응용면역조직화학법화Western blot검측신장색소상피연생인자화전화생장인자-β1단백표체수평.운용t검험화방차분석진행수거통계.결과 여정상대조조비교,당뇨병조대서신소구비대,기저막증후,계막구기질명현증생,부분신소관정공포변성,전화생장인자-β1단백표체수평명현승고(면역조직화학분석:4.60 ±0.14、1.57±0.14,t=3.052,P<0.01;Western blot:1053±64、462±70,t=2.817,P<0.01),이색소상피연생인자단백표체수평현저강저(면역조직화학분석:1.53±0.12、3.96±0.18,t=2.845,P<0.01:Western blot:228±275、698±120,t=3.152,P<0.01).여당뇨병조비교,라격렬동간예조대서신소구비대,기저막증후,계막구기질증생정도명현감경,전화생장인자-β1단백표체수평명현강저(면역조직화학분석:2.79±0.16、4.60±0.14,t=2.964,P<0.01;Western blot:753±81、1053±64,t=2.884,P<0.01),색소상피연생인자단백표체수평현저승고(면역조직화학분석:2.64±0.32、1.53±0.12,t=2.347,P<0.05;Western blot:473±127、228±275,t=2.334,P<0.05).결론 라격렬동가통과하조당뇨병대서신장전화생장인자-β1단백표체、상조색소상피연생인자단백표체래발휘신장보호작용.
Objective To investigate the effect of rosiglitazone on the expression of pigment epithelium-derived factor(PEDF) and transforming growth factor-β1(TGF-β1)in the kidney of diabetic rats.Methods A total of 42 healthy male SD rats(180 to 200g)were randomly assigned to the normal control(NC)group(n=14),diabetes mellitus(DM)group(n=14),and rosiglitazone(RSG)treatment group(n=14).Diabetes was induced by an intraperitoneal injection of 55μ/g streptozotocin.The rats in the RSG group were given rosiglitazone sodium 5μg·g-1·d-1．At the end of 12 weeks，fasting blood glucose,kidney mass,kidney/body mass,24-hour urinary albumin excretion(UAE),serum triglyceride (TG),total cholesterol(TC),low-density lipoprotein cholesterol(LDL-C),very low-density lipoprotein cholesterol(VLDL-C),hish-density lipoprotein cholesterol(HDL-C),BUN,SCr and PEDF were measured.The expression of TGF-β1 and PEDF in the kidney was determined by immunohistochemical analysis and Western blot.Statistical analysis was performed using two-tail Student's t test.Results Compared with the NC group,the DM group was characterized by the glomerular hypertrophy,mesangial expansion and glomerular basement membrane thickening;the protein expression of TGF-β1 was significantly increased(immunohistochemical analysis:4.6±0.14 vs 1.57±0.14,t=3.052,P<0.01:Western blot:1053±64 vs 462±70,t=2.817,P<0.01).whereas the protein expression of PEDF was significantly decreased(immunohistochemical analysis:1.53±0.12 vs 3.96±0.18,t=2.845,P<0.01;Western blot:228±275 vs 698±120,t=3.152,P<0.01)in the DM group.Compared with the DM group,the glomerular hypertrophy, mesangial expansion and glomerular basement membrane thickening were significantly ameliorated in the RGS group;the protein expression of TGF-Bβ1 was significantly lower (immunohistochemical analysis:2.79±0.16 vs 4.60±0.14,t=2.964,P<0.01;Western blot:753 ±81vs1053±64,t=2.884,P<0.01),whereas the protein expression of PEDF was significantly higher (immunohistochemical analysis:2.64±0.32 vs 1.53±0.12,t=2.347,P<0.05;Western blot:473±127 vs 228±275,t=2.334,P<0.05)in the RSG treatment group.Conclusion Renoprotection of rosiglitazone on diabetic rats may be mediated by decreased expression of TGF-β1 and increased expression of PEDF.
