目的 探讨硫酸脱氢表雄酮（DHEAS）对胰岛β细胞株MIN6葡萄糖刺激的胰岛素分泌的影响。方法 以葡萄糖刺激浓度为2.8 mmol/L和16.7 mmol/L的对数生长期MIN6细胞作为实验对象，分别以1、5、10 μmol/L DHEAS干预10 min和24 h（不同浓度DHEAS组），以5 μmol/L DHEAS或与10 μmol/L糖皮质激素受体阻断剂RU486联合干预24 h（DHEAS 和DHEAS+RU486组），设立空白对照组。ELISA法测定细胞培养上清液中胰岛素分泌量，Real-Time PCR检测细胞胰岛素mRNA表达。结果 干预后10 min和24 h时点，5 μmol/L和10 μmol/L DHEAS 组MIN6细胞培养上清液中的胰岛素分泌量均显著高于空白对照组（P<0.05）；干预后24 h时点，DHEAS+RU486组与DHEAS组MIN6细胞培养上清液中胰岛素分泌量比较差异无统计学意义（P>0.05），但均显著高于空白对照组（P<0.05）。干预后24 h时点，5 μmol/L和10 μmol/L DHEAS组MIN6细胞胰岛素mRNA表达均显著高于空白对照组（P<0.05）。结论 DHEAS对MIN6细胞葡萄糖刺激的胰岛素分泌具有促进作用，且其核内信号通路可能不经糖皮质激素受体介导。

Objective To investigate the effects of dehydroepiandrosterone-sulfate (DHEAS) on glucose-stimulated insulin secretion in pancreatic islets β cell lines (MIN6). Methods MIN6 cells at exponential phase of growth stimulated by glucose (2.8 mmol/L and 16.7 mmol/L) were served as study objectives. Cells were treated by DHEAS (1, 5 and 10 μmol/L) for 10 min and 24 h (1 μmol/L DHEAS group, 5 μmol/L DHEAS group and 10 μmol/L DHEAS group), and DHEAS group (treated by 5 μmol/L DHEAS for 24 h) and DHEAS+RU486 group (treated by 5 μmol/L DHEAS+10 μmol/L glucocorticoid receptor blocker RU486 for 24 h) were divided. Besides, blank control group was established. The insulin secretion in the supernatant was measured by ELISA method, and the expression of insulin mRNA was detected by Real-Time PCR. Results After treatment for 10 min and 24 h, the insulin secretion of MIN6 cells in the supernatant in 5 μmol/L DHEAS group and 10 μmol/L DHEAS group was significantly higher than that in blank control group （P<0.05）. After treatment for 24 h, there was no significant difference in insulin secretion of MIN6 cells in the supernatant between DHEAS+RU486 group and DHEAS group (P>0.05), while both were significantly higher than that in blank control group (P<0.05). After treatment for 24 h, the expression of insulin mRNA of MIN6 cells in 5 μmol/L DHEAS group and 10 μmol/L DHEAS group was significantly higher than that in blank control group (P<0.05). Conclusion The glucose-stimulated insulin secretion of MIN6 cells could be promoted by DHEAS, which may be mediated by an unidentified nuclear receptor but not glucocorticoid receptor.