中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2009年
40期
2843-2846
,共4页
单核细胞趋化蛋白1%白介素6%胰岛素受体%内脏脂肪素
單覈細胞趨化蛋白1%白介素6%胰島素受體%內髒脂肪素
단핵세포추화단백1%백개소6%이도소수체%내장지방소
Monocyte chemotactic protein-1%Interleukin-6%Insulin receptor%Visfatin
目的 探讨内脏脂肪素是否能调节内皮细胞单核细胞趋化蛋白1(MCP-1)和白介素6(IL-6)生成以及胰岛素受体(IR)的介导作用.方法 不同剂量和不同干预时间的内脏脂肪素刺激3～5代脐静脉内皮细胞(HUVEC);然后在内脏脂肪素(100 ng/m1)刺激基础上加入IR酪氨酸激酶抑制剂预处理HUVEC,24 h后测定MCP-1和IL-6蛋白和基因表达.酶联免疫吸附法和实时定量聚合酶链反应检测MCP-1和IL-6蛋白和mRNA表达.结果 内脏脂肪素剂量和时间依赖性促进HUVEC合成MCP-1[剂量效应:对照组:(62±10) pg/ml、100 ng/ml:(273±65) pg/ml、500 ng/ml:(1630±103) pg/ml;时间效应:对照组:(37±27) pg/ml、12 h:(184±56) pg/ml、48 h:(328±80) pg/ml]和IL-6[剂量效应:对照组:(31.8±1.7) pg/ml、100 ng/ml:(42.5±5.7) Pg/ml、500 ng/ml:(154.7±10.2) pg/ml;时间效应:对照组:(15.7±3.4) pg/ml、12 h:(35.4±4.7) pg/ml、48 h:(77.6±11.8) pg/ml].IR酩氨酸激酶抑制剂抑制内脏脂肪素诱导的MCP和IL-6蛋白和基因表达.结论 内脏脂肪索能诱导HUVEC合成和分泌MCP-1、IL-6,其作用通过IR信号通路介导.
目的 探討內髒脂肪素是否能調節內皮細胞單覈細胞趨化蛋白1(MCP-1)和白介素6(IL-6)生成以及胰島素受體(IR)的介導作用.方法 不同劑量和不同榦預時間的內髒脂肪素刺激3～5代臍靜脈內皮細胞(HUVEC);然後在內髒脂肪素(100 ng/m1)刺激基礎上加入IR酪氨痠激酶抑製劑預處理HUVEC,24 h後測定MCP-1和IL-6蛋白和基因錶達.酶聯免疫吸附法和實時定量聚閤酶鏈反應檢測MCP-1和IL-6蛋白和mRNA錶達.結果 內髒脂肪素劑量和時間依賴性促進HUVEC閤成MCP-1[劑量效應:對照組:(62±10) pg/ml、100 ng/ml:(273±65) pg/ml、500 ng/ml:(1630±103) pg/ml;時間效應:對照組:(37±27) pg/ml、12 h:(184±56) pg/ml、48 h:(328±80) pg/ml]和IL-6[劑量效應:對照組:(31.8±1.7) pg/ml、100 ng/ml:(42.5±5.7) Pg/ml、500 ng/ml:(154.7±10.2) pg/ml;時間效應:對照組:(15.7±3.4) pg/ml、12 h:(35.4±4.7) pg/ml、48 h:(77.6±11.8) pg/ml].IR酩氨痠激酶抑製劑抑製內髒脂肪素誘導的MCP和IL-6蛋白和基因錶達.結論 內髒脂肪索能誘導HUVEC閤成和分泌MCP-1、IL-6,其作用通過IR信號通路介導.
목적 탐토내장지방소시부능조절내피세포단핵세포추화단백1(MCP-1)화백개소6(IL-6)생성이급이도소수체(IR)적개도작용.방법 불동제량화불동간예시간적내장지방소자격3～5대제정맥내피세포(HUVEC);연후재내장지방소(100 ng/m1)자격기출상가입IR락안산격매억제제예처리HUVEC,24 h후측정MCP-1화IL-6단백화기인표체.매련면역흡부법화실시정량취합매련반응검측MCP-1화IL-6단백화mRNA표체.결과 내장지방소제량화시간의뢰성촉진HUVEC합성MCP-1[제량효응:대조조:(62±10) pg/ml、100 ng/ml:(273±65) pg/ml、500 ng/ml:(1630±103) pg/ml;시간효응:대조조:(37±27) pg/ml、12 h:(184±56) pg/ml、48 h:(328±80) pg/ml]화IL-6[제량효응:대조조:(31.8±1.7) pg/ml、100 ng/ml:(42.5±5.7) Pg/ml、500 ng/ml:(154.7±10.2) pg/ml;시간효응:대조조:(15.7±3.4) pg/ml、12 h:(35.4±4.7) pg/ml、48 h:(77.6±11.8) pg/ml].IR명안산격매억제제억제내장지방소유도적MCP화IL-6단백화기인표체.결론 내장지방색능유도HUVEC합성화분비MCP-1、IL-6,기작용통과IR신호통로개도.
Objective Visfatin is a new novel proinflammatory adipoeytokine affecting insulin resistance by binding to insulin receptor.To investigate whether visfatin stimulates monoeyte chemotaetic protein-1 (MCP-1) and interleukin-6 (IL-6) production in human umbilical vein endothelial cells (HUVEC) and mediates insulin receptor (IR) is involved in are not known.Methods Cultured HUVEC was treated with different doses and durations of visfatin.Furthermore,HUVEC was pretreated with hydroxy2-naphthalenylmethylphosphonic acid trisaeetoxymethyl ester (HNMPA-(AM)3),a specific inhibitor of IR followed by visfatin (100 ng/ml) treatment.Enzyme-linked immunosorbent assay (ELISA) were used to measure MCP-1 and IL-6 production in HUVEC.Real-time quantitative reverse-transcription polymerase chain reaction (RT-PCR) was used for determining MCP-1 and IL-6 mRNA expression.Results Visfatin significantly dose- and time-dependently up-regulated protein production of MCP-1 and IL-6 in HUVEC.We therefore found visfatin-induced MCP-1 and IL-6 production and gene expression in HUVEC were inhibited by HNMPA-(AM)3.Condusion Visfatin induces endothelial MCP-1 and IL-6 production in HUVEC in a dose and time-dependently manner.This action appears to be mediated via insulin receptor pathway.
