临床药物治疗杂志
臨床藥物治療雜誌
림상약물치료잡지
CLINICAL MEDICATION JOURNAL
2013年
2期
14-17
,共4页
周赛君%王洁%孟振兴%陈思思%于德民%于佩**
週賽君%王潔%孟振興%陳思思%于德民%于珮**
주새군%왕길%맹진흥%진사사%우덕민%우패**
第V结构域缺失型β2-糖蛋白I%糖尿病肾病%VEGF-NO轴%尿蛋白
第V結構域缺失型β2-糖蛋白I%糖尿病腎病%VEGF-NO軸%尿蛋白
제V결구역결실형β2-당단백I%당뇨병신병%VEGF-NO축%뇨단백
domain V deletion ofβ2-glycoprotein I%diabetic nephropathy%VEGF-NO axis%urinary protein
目的:探讨第V结构域缺失型β2-糖蛋白I( DI-IV)对糖尿病大鼠24h尿蛋白排泄以及血管内皮生长因子(VEGF)-一氧化氮(NO)轴的影响.方法:将大鼠高脂喂养8周后尾静脉注射STZ(30mg?kg-1)进行糖尿病造模,造模成功1周后将大鼠随机分为对照组、β2糖蛋白I(β2-GPI)组以及DI-IV组,每周分别于尾静脉注射人血清白蛋白(HSA)、β2-GPI、DI-IV各200mg?kg-1,持续4周.于干预前后取血,测定血肌酐(Scr)、尿素氮(BUN)、血甘油三酯(TG)、总胆固醇酯(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、24h尿白蛋等.采用Western blot检测肾脏VEGF、内皮源性一氧化氮合酶(eNOS)的表达及eNOS磷酸化.结果:与干预前相比,对照组、β2-GPI组TG、TC、LDL-C、HDL-C、Scr无明显变化(P均>0.05),而血糖、24h尿蛋白排泄升高(P均<0.05);干预后DI-IV组血TC、LDL-C、24h尿蛋白排泄均减少(P均<0.05).与对照相比,DI-IV组肾脏VEGF-A表达减少(P<0.05),eNOS的磷酸化表达增加(P<0.05).结论:DI-IV可能通过改善糖尿病大鼠肾脏VEGF-NO轴功能以及降脂作用,减轻糖尿病SD大鼠24h尿蛋白的排泄.
目的:探討第V結構域缺失型β2-糖蛋白I( DI-IV)對糖尿病大鼠24h尿蛋白排洩以及血管內皮生長因子(VEGF)-一氧化氮(NO)軸的影響.方法:將大鼠高脂餵養8週後尾靜脈註射STZ(30mg?kg-1)進行糖尿病造模,造模成功1週後將大鼠隨機分為對照組、β2糖蛋白I(β2-GPI)組以及DI-IV組,每週分彆于尾靜脈註射人血清白蛋白(HSA)、β2-GPI、DI-IV各200mg?kg-1,持續4週.于榦預前後取血,測定血肌酐(Scr)、尿素氮(BUN)、血甘油三酯(TG)、總膽固醇酯(TC)、低密度脂蛋白膽固醇(LDL-C)、高密度脂蛋白膽固醇(HDL-C)、24h尿白蛋等.採用Western blot檢測腎髒VEGF、內皮源性一氧化氮閤酶(eNOS)的錶達及eNOS燐痠化.結果:與榦預前相比,對照組、β2-GPI組TG、TC、LDL-C、HDL-C、Scr無明顯變化(P均>0.05),而血糖、24h尿蛋白排洩升高(P均<0.05);榦預後DI-IV組血TC、LDL-C、24h尿蛋白排洩均減少(P均<0.05).與對照相比,DI-IV組腎髒VEGF-A錶達減少(P<0.05),eNOS的燐痠化錶達增加(P<0.05).結論:DI-IV可能通過改善糖尿病大鼠腎髒VEGF-NO軸功能以及降脂作用,減輕糖尿病SD大鼠24h尿蛋白的排洩.
목적:탐토제V결구역결실형β2-당단백I( DI-IV)대당뇨병대서24h뇨단백배설이급혈관내피생장인자(VEGF)-일양화담(NO)축적영향.방법:장대서고지위양8주후미정맥주사STZ(30mg?kg-1)진행당뇨병조모,조모성공1주후장대서수궤분위대조조、β2당단백I(β2-GPI)조이급DI-IV조,매주분별우미정맥주사인혈청백단백(HSA)、β2-GPI、DI-IV각200mg?kg-1,지속4주.우간예전후취혈,측정혈기항(Scr)、뇨소담(BUN)、혈감유삼지(TG)、총담고순지(TC)、저밀도지단백담고순(LDL-C)、고밀도지단백담고순(HDL-C)、24h뇨백단등.채용Western blot검측신장VEGF、내피원성일양화담합매(eNOS)적표체급eNOS린산화.결과:여간예전상비,대조조、β2-GPI조TG、TC、LDL-C、HDL-C、Scr무명현변화(P균>0.05),이혈당、24h뇨단백배설승고(P균<0.05);간예후DI-IV조혈TC、LDL-C、24h뇨단백배설균감소(P균<0.05).여대조상비,DI-IV조신장VEGF-A표체감소(P<0.05),eNOS적린산화표체증가(P<0.05).결론:DI-IV가능통과개선당뇨병대서신장VEGF-NO축공능이급강지작용,감경당뇨병SD대서24h뇨단백적배설.
@@@@Objective:To investigate effect of domain V deletion of β2-glycoprotein Ⅰ (DI-IV) on 24-hour urinary protein excretion ,VEGF-NO axis,and possible mechanisms in diabetic rats.Methods:Diabetic model was established with the use of SD rats, treated with intravenous injection of STZ (30mg/kg) after a high fat diet for eight weeks. One week after successful modeling, the rats were randomly assigned to control group, β2 glycoprotein I (β2-GPI) group and DI-IV group, treated with intravenous injection of human serum albumin (HSA), β2-GPI or DI-IV with a dose of 200mg/kg every week ,for four weeks, respectively. Blood samples were taken before and after the intervention, and serum creatinine (Scr), blood urea nitrogen (BUN), serum triglyceride (TG), total cholesterol ester (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and 24-hour urinary protein were analyzed . Western blot was used to analyze the expression of VEGF and endothelial nitric oxide synthase (eNOS), and the phosphorylation of eNOS of rats’ kidneys.Results:After intervention,TG,TC,HDL-C,Scr and LDL-C had no significant difference (p> 0.05) while blood glucose and 24-hour urinary protein excretion increased (p <0.05) in control group and β2-GPI group;TC,LDL-C, 24-hour urinary protein excretion decreased (p<0.05) in DI-IV group. VEGF-A expression in kidneys decreased more and phosphorylation of eNOS increased more in DI-IV group than in control group (p <0.05) . Conclusion:DI-IV could relieve 24-hour urine protein excretion of diabetic SD rats. Possible mechanisms are to improve VEGF-NO axis function and lipid-lowering effect in diabetic rat kidneys.