科技通报
科技通報
과기통보
Bulletin of Science and Technology
2015年
10期
31-33
,共3页
地塞米松%胰岛素抵抗%HepG2%3T3-L1%C2C12
地塞米鬆%胰島素牴抗%HepG2%3T3-L1%C2C12
지새미송%이도소저항%HepG2%3T3-L1%C2C12
dexamethasone%insulin resistance%hepG2. 3 t3-L1%C2C12
目的:探讨在体外建立方便可靠的肝胰岛素抵抗细胞模型、脂肪细胞胰岛素抵抗模型和肌细胞胰岛素抵抗模型的方法.方法:3T3-L1小鼠前脂肪细胞、C2C12小鼠成肌细胞分别诱导分化为成熟的脂肪细胞和肌细胞.采用地塞米松(EDX)诱导人肝细胞HepG2以及分化成熟的HepG2、C2C12细胞,以葡萄糖氧化酶法检测细胞对葡萄糖的消耗情况.结果:1μmol/L DEX作用24 h和48 h均能抑制细胞葡萄糖消耗,撤掉DEX,胰岛素抵抗细胞模型在48 h内维持稳定.对于HepG2和C2C12细胞,DEX造模48 h优于24 h;但对于3T3-L1细胞,DEX造模24 h和48 h对细胞葡萄糖消耗影响无显著性差异.结论:DEX可诱导3T3-L1、HepG2、C2C12细胞产生胰岛素抵抗,这种细胞模型简便稳定.
目的:探討在體外建立方便可靠的肝胰島素牴抗細胞模型、脂肪細胞胰島素牴抗模型和肌細胞胰島素牴抗模型的方法.方法:3T3-L1小鼠前脂肪細胞、C2C12小鼠成肌細胞分彆誘導分化為成熟的脂肪細胞和肌細胞.採用地塞米鬆(EDX)誘導人肝細胞HepG2以及分化成熟的HepG2、C2C12細胞,以葡萄糖氧化酶法檢測細胞對葡萄糖的消耗情況.結果:1μmol/L DEX作用24 h和48 h均能抑製細胞葡萄糖消耗,撤掉DEX,胰島素牴抗細胞模型在48 h內維持穩定.對于HepG2和C2C12細胞,DEX造模48 h優于24 h;但對于3T3-L1細胞,DEX造模24 h和48 h對細胞葡萄糖消耗影響無顯著性差異.結論:DEX可誘導3T3-L1、HepG2、C2C12細胞產生胰島素牴抗,這種細胞模型簡便穩定.
목적:탐토재체외건립방편가고적간이도소저항세포모형、지방세포이도소저항모형화기세포이도소저항모형적방법.방법:3T3-L1소서전지방세포、C2C12소서성기세포분별유도분화위성숙적지방세포화기세포.채용지새미송(EDX)유도인간세포HepG2이급분화성숙적HepG2、C2C12세포,이포도당양화매법검측세포대포도당적소모정황.결과:1μmol/L DEX작용24 h화48 h균능억제세포포도당소모,철도DEX,이도소저항세포모형재48 h내유지은정.대우HepG2화C2C12세포,DEX조모48 h우우24 h;단대우3T3-L1세포,DEX조모24 h화48 h대세포포도당소모영향무현저성차이.결론:DEX가유도3T3-L1、HepG2、C2C12세포산생이도소저항,저충세포모형간편은정.
Objective:To investigate the establish a convenient and reliable hepatic insulin resistance in vitro cell model, the fat cells insulin resistance model and the method of muscle insulin resistance model. Methods:3 t3-L1 before the fat cells in mice, mice C2C12 myoblast differentiation into mature fat cells and muscle cells. Using dexamethasone (EDX) in-duced liver cell HepG2 and matured HepG2, C2C12 cells, with glucose oxidase method to detect the cell to glucose con-sumption situation. Results:1 mu mol/L DEX effect can inhibit cell 24 h and 48 h glucose consumption, remove DEX, in-sulin resistance stability of the cell model within 48 h. In HepG2 and C2C12 cells, 24 h, 48 h DEX made model is superior to the But for the 3 t3 cells-L1, DEX building 24 h and 48 h there was no significant difference effect on cell glucose con-sumption. Conclusion:DEX can induce 3 t3-L1, HepG2, C2C12 cells produce insulin resistance, the cell model is sim-ple and stable.
