上海交通大学学报（医学版）
上海交通大學學報（醫學版）
상해교통대학학보（의학판）
JOURNAL OF SHANGHAI JIAOTONG UNIVERSITY(MEDICAL SCIENCE)
2010年
4期
390-393
,共4页
徐茜%张志国%金丽娜%石国军%杨洋%田秀丽%张杉杉%崔斌%汤正义%宁光
徐茜%張誌國%金麗娜%石國軍%楊洋%田秀麗%張杉杉%崔斌%湯正義%寧光
서천%장지국%금려나%석국군%양양%전수려%장삼삼%최빈%탕정의%저광
葡萄糖%血管紧张素Ⅱ受体%罗格列酮%脂肪细胞
葡萄糖%血管緊張素Ⅱ受體%囉格列酮%脂肪細胞
포도당%혈관긴장소Ⅱ수체%라격렬동%지방세포
glucose%angiotesin Ⅱ receptor%rosiglitazone%adipocytes
目的 研究不同浓度葡萄糖培养环境及罗格列酮干预对分化成熟脂肪细胞血管紧张素Ⅱ受体1(ATIR)和受体2(AT2R)基因表达的影响.方法 取分化成熟的脂肪细胞3T3-L1,分别用含不同浓度葡萄糖(空白对照、5.6、11.2、25.0 mmol/L)的培养基和含不同浓度葡萄糖并添加10 nmol/L罗格列酮的培养基分组培养24 h,Real-time PCR检测3T3-L1脂肪细胞AT1R和AT2R基因表达.结果 5.6 mmol/L葡萄糖处理组AT1R基因表达明显低于空白对照和11.2、25.0 mmol/L葡萄糖处理组(P<0.05);AT2R基因表达随着葡萄糖浓度的升高而明显上调(P<0.05).随着葡萄糖浓度的升高,罗格列酮干预组AT1R和AT2R基因表达呈下降趋势.与相应浓度的葡萄糖处理组比较,罗格列酮干预组AT1R表达均显著上调(P<0.05).作用随葡萄糖浓度的升高而减弱;AT2R基因表达显著下调(P<0.05),作用随葡萄糖浓度的升高而加强.结论 罗格列酮对高浓度葡萄糖导致的脂肪细胞AT1R和AT2R基因表达变化具有调控作用.
目的 研究不同濃度葡萄糖培養環境及囉格列酮榦預對分化成熟脂肪細胞血管緊張素Ⅱ受體1(ATIR)和受體2(AT2R)基因錶達的影響.方法 取分化成熟的脂肪細胞3T3-L1,分彆用含不同濃度葡萄糖(空白對照、5.6、11.2、25.0 mmol/L)的培養基和含不同濃度葡萄糖併添加10 nmol/L囉格列酮的培養基分組培養24 h,Real-time PCR檢測3T3-L1脂肪細胞AT1R和AT2R基因錶達.結果 5.6 mmol/L葡萄糖處理組AT1R基因錶達明顯低于空白對照和11.2、25.0 mmol/L葡萄糖處理組(P<0.05);AT2R基因錶達隨著葡萄糖濃度的升高而明顯上調(P<0.05).隨著葡萄糖濃度的升高,囉格列酮榦預組AT1R和AT2R基因錶達呈下降趨勢.與相應濃度的葡萄糖處理組比較,囉格列酮榦預組AT1R錶達均顯著上調(P<0.05).作用隨葡萄糖濃度的升高而減弱;AT2R基因錶達顯著下調(P<0.05),作用隨葡萄糖濃度的升高而加彊.結論 囉格列酮對高濃度葡萄糖導緻的脂肪細胞AT1R和AT2R基因錶達變化具有調控作用.
목적 연구불동농도포도당배양배경급라격렬동간예대분화성숙지방세포혈관긴장소Ⅱ수체1(ATIR)화수체2(AT2R)기인표체적영향.방법 취분화성숙적지방세포3T3-L1,분별용함불동농도포도당(공백대조、5.6、11.2、25.0 mmol/L)적배양기화함불동농도포도당병첨가10 nmol/L라격렬동적배양기분조배양24 h,Real-time PCR검측3T3-L1지방세포AT1R화AT2R기인표체.결과 5.6 mmol/L포도당처리조AT1R기인표체명현저우공백대조화11.2、25.0 mmol/L포도당처리조(P<0.05);AT2R기인표체수착포도당농도적승고이명현상조(P<0.05).수착포도당농도적승고,라격렬동간예조AT1R화AT2R기인표체정하강추세.여상응농도적포도당처리조비교,라격렬동간예조AT1R표체균현저상조(P<0.05).작용수포도당농도적승고이감약;AT2R기인표체현저하조(P<0.05),작용수포도당농도적승고이가강.결론 라격렬동대고농도포도당도치적지방세포AT1R화AT2R기인표체변화구유조공작용.
Objective To investigate the effects of different glucose concentrations and rosiglitazone intervention on expression of angiotension fl receptor 1 ( ATI R) and angiotension II receptor 2 ( AT2R) genes in differentiated mature adipocytes. Methods Differentiated mature 3T3-L1 adipocytes were cultured in media with different concentrations of glucose (blank control, 5.6 mmol/L, 11.2 mmol/L and 25.0 mmol/L) and media with different concentrations of glucose and 10 nmol/L rosiglitazone for 24 h. Real-time PCR was employed to detect the expression of AT1R and AT2R genes in 3T3-Ll adipocytes. Results The expression of AT1R gene was significantly lower in 5.6 mmol/L glucose treatment group than that in blank control group, 11.2 mmol/L glucose treatment group and 25.0 mmol/L glucose treatment group (P<0.05), and the expression of AT2R gene significantly increased with the increase of glucose concentrations (P < 0. 05). The expression of AT1R and AT2R genes in rosiglitazone intervention group decreased with the increase of glucose concentrations. Compared with corresponding glucose treatment groups, the expression of ATI R gene in rosiglitazone intervention groups was significantly up-regulated (P < 0. 05), with the effect decreasing gradually with the increase of glucose concentrations, and the expression of AT2R gene was significantly down-regulated (P < 0. 05), with the effect increasing with the increase of glucose concentrations. Conclusion Rosiglitazone plays a regulatory role in the expression of ATI R and AT2R genes in adipocytes under high concentrations of glucose.
