CAJ | 학술논문

实验旨在研究糖皮质激素快速、非基因组作用的细胞内信号传导机制.Western分析研究结果表明, 皮质酮可快速激活PC12细胞中p38丝列原激活的蛋白激酶(mitogen-activated protein kinase, MAPK), 时间、浓度曲线均为钟形, 最大激活为10-9 mol/L 和15 min.糖皮质激素受体阻断剂RU38486不能阻断此作用, 而小牛血清白蛋白耦联的皮质酮也能快速激活p38.受体酪氨酸激酶阻断剂genistein 对此作用无影响, 表明此快速作用不涉及受体酪氨酸激酶活性.此作用能被蛋白激酶C (protein kinase C, PKC)激动剂PMA模拟, 而被PKC阻断剂G6976所阻断.结果表明, 皮质酮可能通过推测的膜受体以PKC依赖的方式快速激活p38 MAPK.
실험지재연구당피질격소쾌속、비기인조작용적세포내신호전도궤제.Western분석연구결과표명, 피질동가쾌속격활PC12세포중p38사렬원격활적단백격매(mitogen-activated protein kinase, MAPK), 시간、농도곡선균위종형, 최대격활위10-9 mol/L 화15 min.당피질격소수체조단제RU38486불능조단차작용, 이소우혈청백단백우련적피질동야능쾌속격활p38.수체락안산격매조단제genistein 대차작용무영향, 표명차쾌속작용불섭급수체락안산격매활성.차작용능피단백격매C (protein kinase C, PKC)격동제PMA모의, 이피PKC조단제G6976소조단.결과표명, 피질동가능통과추측적막수체이PKC의뢰적방식쾌속격활p38 MAPK.
The present study using immunoblot showed that corticosterone (B) could induce a rapid activation of p38 in PC12 cells. The dose- and time-response curves were bell-shaped with a maximal activation at 10－9 mol/L and 15 min respectively. The activation was not affected by steroid nuclear receptor antagonist RU38486. Bovine serum albumin coupled B (B-BSA) could induce phosphorylation of p38. Tyrosine kinase inhibitor genistein failed to block the phosphorylation, a fact suggesting that the tyrosine kinase activity is not involved in the pathway. On the other hand, phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, could mimic the actions of B, while G6976, a PKC inhibitor, could completely abolish the phosphorylation induced by B. These results clearly demonstrate that B activates p38 MAPK readily via a putative membrane receptor through a PKC-dependent pathway.