CAJ | 학술논문

目的从蛋白激酶C(PKC)信号通路角度,探讨游离脂肪酸(FFA)引起肝脏胰岛素抵抗(IR)的可能机制.方法培养HepG2细胞,同时设立对照组、软脂酸(PA)组、高胰岛素组.软脂酸组、高胰岛素组分别用250 μmol/L PA、5×10-7mol/L胰岛素处理24 h.然后对照组、软脂酸组再根据胰岛素刺激前加(+)与不加(-)PKC抑制剂白屈菜红碱盐酸盐(chelerythrine chloride,CC)5 μmol/L预处理1h,随机分为两亚组:对照组(-)、对照组(+)、PA组(-)、PA组(+).葡萄糖氧化酶法测定胰岛素刺激后12 h葡萄糖消耗量,蒽酮法测定胰岛素刺激后3 h点细胞内糖原含量,Western blotting技术检测15 min点细胞内P-Ser473 PKB、P-Set21/9 GSK-3α/β水平.结果 PA组(-)与高胰岛素组葡萄糖消耗量无统计学差异(P=0.523).葡萄糖消耗量、细胞内糖原含量、P-Ser473 PKB、P-Ser21 GSK-3α、P-Ser9 GSK-3β水平均显示,PA组(-)与对照组(-)比较显著降低(P值依次为0.000,0.000,0.004,0.004,0.028),对照组(+)与对照组(-)比较略有升高但无显著性差异;PA组(+)与PA组(-)比较显著升高(P值依次为0.000,0.014,0.043,0.041,0.035).结论 PA(250 μmol/L)体外成功诱导了HepG2细胞产生IR,PKC信号通路在FFA引起肝脏IR中起着重要作用.
목적 종단백격매C(PKC)신호통로각도,탐토유리지방산(FFA)인기간장이도소저항(IR)적가능궤제.방법 배양HepG2세포,동시설립대조조、연지산(PA)조、고이도소조.연지산조、고이도소조분별용250 μmol/L PA、5×10-7mol/L이도소처리24 h.연후대조조、연지산조재근거이도소자격전가(+)여불가(-)PKC억제제백굴채홍감염산염(chelerythrine chloride,CC)5 μmol/L예처리1h,수궤분위량아조:대조조(-)、대조조(+)、PA조(-)、PA조(+).포도당양화매법측정이도소자격후12 h포도당소모량,은동법측정이도소자격후3 h점세포내당원함량,Western blotting기술검측15 min점세포내P-Ser473 PKB、P-Set21/9 GSK-3α/β수평.결과 PA조(-)여고이도소조포도당소모량무통계학차이(P=0.523).포도당소모량、세포내당원함량、P-Ser473 PKB、P-Ser21 GSK-3α、P-Ser9 GSK-3β수평균현시,PA조(-)여대조조(-)비교현저강저(P치의차위0.000,0.000,0.004,0.004,0.028),대조조(+)여대조조(-)비교략유승고단무현저성차이;PA조(+)여PA조(-)비교현저승고(P치의차위0.000,0.014,0.043,0.041,0.035).결론 PA(250 μmol/L)체외성공유도료HepG2세포산생IR,PKC신호통로재FFA인기간장IR중기착중요작용.