中国医科大学学报
中國醫科大學學報
중국의과대학학보
JOURNAL OF CHINA MEDICAL UNIVERSITY
2009年
10期
741-744
,共4页
胰岛素抵抗%脂联素%替米沙坦
胰島素牴抗%脂聯素%替米沙坦
이도소저항%지련소%체미사탄
insulin resistance%adiponectin%telmisarlan
目的 探讨替米沙坦对胰岛素抵抗大鼠肾脏脂联素(APN)表达的影响.方法 采用高脂饲料喂养10周建立胰岛素抵抗大鼠模型,并用正常血糖一高血浆胰岛素钳夹技术评估.光镜及电镜行肾脏形态学检查,逆转录聚合酶链反应方法测定APNmRNA表达,免疫组化染色观察APN蛋白水平变化.结果 胰岛素抵抗大鼠肾脏APN mRNA和蛋白表达明显低于正常对照组(P均<0.05),同时大鼠肾脏出现病理变化;替米沙坦干预后,肾组织APN mRNA和蛋白表达较胰岛素抵抗组升高(P均<0.05),同时肾脏病理变化也得到明显改善.结论 替米沙坦可能通过调节肾脏APN的表达,起到保护胰岛素抵抗相关的肾脏损伤的作用.
目的 探討替米沙坦對胰島素牴抗大鼠腎髒脂聯素(APN)錶達的影響.方法 採用高脂飼料餵養10週建立胰島素牴抗大鼠模型,併用正常血糖一高血漿胰島素鉗夾技術評估.光鏡及電鏡行腎髒形態學檢查,逆轉錄聚閤酶鏈反應方法測定APNmRNA錶達,免疫組化染色觀察APN蛋白水平變化.結果 胰島素牴抗大鼠腎髒APN mRNA和蛋白錶達明顯低于正常對照組(P均<0.05),同時大鼠腎髒齣現病理變化;替米沙坦榦預後,腎組織APN mRNA和蛋白錶達較胰島素牴抗組升高(P均<0.05),同時腎髒病理變化也得到明顯改善.結論 替米沙坦可能通過調節腎髒APN的錶達,起到保護胰島素牴抗相關的腎髒損傷的作用.
목적 탐토체미사탄대이도소저항대서신장지련소(APN)표체적영향.방법 채용고지사료위양10주건립이도소저항대서모형,병용정상혈당일고혈장이도소겸협기술평고.광경급전경행신장형태학검사,역전록취합매련반응방법측정APNmRNA표체,면역조화염색관찰APN단백수평변화.결과 이도소저항대서신장APN mRNA화단백표체명현저우정상대조조(P균<0.05),동시대서신장출현병리변화;체미사탄간예후,신조직APN mRNA화단백표체교이도소저항조승고(P균<0.05),동시신장병리변화야득도명현개선.결론 체미사탄가능통과조절신장APN적표체,기도보호이도소저항상관적신장손상적작용.
Objective To investigate the influences of telmiaartan on renal expression of adiponectin (APN) in insulin resistance rats. Methods Insulin resistance rat model was induced by long-term high-fat feeding and was assessed by euglycemic-hyperinsulinemia clamp technique. The morphological changes of the kidney lissue were observed by the light and electronic microscopy.Glomerular APN mRNA ex-pression and protein synthesis were evaluated by the reveree transcription polymerase chain reaction and immunohistochemical staining re-spectively. Results Both APN mRNA and APN protein were lower in insulin resistance rats than those in control rats (P < 0.05). More-over, the main features of the renal parenchyma were observed in insulin resistance rats. The expression levels of APN mRNA and APN pro-tein were increased after the treatment with lelmisartan (P <0.05). The renal damage was significantly reduced as well. Conclusion The up-regulation of APN expression induced by telmisartan might prevent the renal damage of insulin resistance.