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目的 探讨CalpaininhibitorⅠ对糖皮质激素受体 (glucocorticoidreceptor ,GR)表达和转录激活作用的影响。方法 Raw 2 64 .7细胞经地塞米松、CalpaininhibitorⅠ或两者共同处理 12h ,观察糖皮质激素受体表达水平的变化。质粒PRsh GRα和报告质粒pMAMneo CAT转入COS 7细胞 ,观察CalpaininhibitorⅠ对糖皮质激素受体转录激活作用的影响。结果 Raw 2 64 .7细胞经地塞米松处理 12h后GR蛋白条带减弱 ,提示地塞米松可诱导GR表达下调 ,而CalpaininhibitorⅠ可以部分抑制此作用。共转染实验表明CalpaininhibitorⅠ可增强地塞米松对GR的转录激活作用。结论 CalpaininhibitorⅠ可抑制糖皮质激素受体 (激素依赖性受体 )下调 ,并可增强GR的转录激活作用。
Objective To investigate the effect of Calpaininhibitor Ⅰ on the expression and transcriptional activation of glucocorticoid receptor (GR). Methods Raw 2 647 cells were treated with dexamethasone, Calpaininhibitor Ⅰ or both for 12 hours to observe the changes of glucocorticoid receptor expression. The plasmid PRsh GRα and the reporter plasmid pMAMneo CAT were transfected into COS 7 cells to observe the effect of Calpaininhibitor Ⅰ on the transcriptional activation of glucocorticoid receptor. Results Degraded RAW264.7 cells treated with dexamethasone for 12 h attenuated the expression of GR protein, which suggested that dexamethasone induced a down-regulation of GR expression, whereas Calpain inhibitor I partially inhibited this effect. Co-transfection experiments show that Calpaininhibitor Ⅰ can enhance dexamethasone on GR transcriptional activation. Conclusion Calpain inhibitor I can inhibit the down-regulation of glucocorticoid receptor (hormone-dependent receptor) and enhance the transcriptional activation of GR.