低剂量姜黄素通过糖皮质激素受体和 STAT3 刺激大鼠胚胎神经干细胞的增殖。
Low-dose curcumin stimulates proliferation of rat embryonic neural stem cells through glucocorticoid receptor and STAT3.
机构信息
Department of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Zhejiang Province Key Lab of Anesthesiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
出版信息
CNS Neurosci Ther. 2018 Oct;24(10):940-946. doi: 10.1111/cns.12843. Epub 2018 Mar 12.
AIMS
This study was to determine whether curcumin had any effect on the proliferation of neural stem cell (NSC), analyze the expression of glucocorticoid receptor (GR), signal transducer and activator of transcription 3 (STAT3), and Notch1 at transcription and protein level, and discuss the related mechanisms.
METHODS AND RESULTS
NSCs were harvested from E15 SD rat brain and cultured. All experiments were performed at the second passage. Cell cytotoxicity, cell viability, and proliferation assays were used to figure out the optimal concentration of curcumin, which can be used for the protein and mRNA studies. The results showed that by downregulation of GR and STAT3 expression, 0.5 μmol L curcumin exhibited the most pronounced effect in promoting the proliferation of NSCs, which were also induced by antagonists of GR and STAT3, but was inhibited by GR agonist.
CONCLUSION
This study shows that low-dose curcumin stimulates the proliferation of NSCs, which is probably by inhibiting the mRNA and protein expressions of GR and directly or indirectly regulating the STAT3 via the synergistic effect of GR and STAT3 pathways and its related signal pathways.
目的
本研究旨在探讨姜黄素对神经干细胞（NSC）增殖的影响，分析其在转录和蛋白水平上对糖皮质激素受体（GR）、信号转导和转录激活因子 3（STAT3）和 Notch1 的表达情况，并探讨其相关机制。
方法和结果
从 E15 天 SD 大鼠脑中分离培养 NSCs，进行细胞毒性、细胞活力和增殖实验，以确定用于蛋白质和 mRNA 研究的最佳姜黄素浓度。结果表明，通过下调 GR 和 STAT3 的表达，0.5μmol·L-1 的姜黄素在促进 NSCs 增殖方面表现出最显著的效果，GR 和 STAT3 的拮抗剂也能诱导其增殖，但 GR 激动剂则抑制其增殖。
结论
本研究表明，低剂量姜黄素可刺激 NSCs 的增殖，这可能是通过抑制 GR 和 STAT3 的 mRNA 和蛋白表达，通过 GR 和 STAT3 途径及其相关信号途径的协同作用，直接或间接调节 STAT3。
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