Ghoumari A M, Dusart I, El-Etr M, Tronche F, Sotelo C, Schumacher M, Baulieu E-E
Institut National de la Santé et de la Recherche Médicale U488, Batiment Gregory Pincus, 80 Rue du Général Leclerc, 94276 Kremlin-Bicêtre, France.
Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7953-8. doi: 10.1073/pnas.1332667100. Epub 2003 Jun 16.
Mifepristone (RU486), which binds with high affinity to both progesterone and glucocorticosteroid receptors (PR and GR), is well known for its use in the termination of unwanted pregnancy, but other activities including neuroprotection have been suggested. Cerebellar organotypic cultures from 3 to 7 postnatal day rat (P3-P7) were studied to examine the neuroprotective potential of RU486. In such cultures, Purkinje cells enter a process of apoptosis with a maximum at P3. This study shows that RU486 (20 microM) can protect Purkinje cells from this apoptotic process. The neuroprotective effect did involve neither PR nor GR, because it could not be mimicked or inhibited by other ligands of these receptors, and because it still took place in PR mutant (PR-KO) mice and in brain-specific GR mutant mice (GRNes/Cre). Potent antioxidant agents did not prevent Purkinje cells from this developmental cell death. The neuroprotective effect of RU486 could also be observed in pathological Purkinje cell death. Indeed, this steroid is able to prevent Purkinje cells from death in organotypic cultures of cerebellar slices from Purkinje cell degeneration (pcd) mutant mice, a murine model of hereditary neurodegenerative ataxia. In P0 cerebellar slices treated with RU486 for 6 days and further kept in culture up to 21 days, the synthetic steroid increased by 16.2-fold the survival of pcd/pcd Purkinje cells. Our results show that RU486 may act through a new mechanism, not yet elucidated, to protect Purkinje cells from death.
米非司酮(RU486)能与孕激素和糖皮质激素受体(PR和GR)高亲和力结合,因其用于终止意外妊娠而广为人知,但也有人提出它还有其他活性,包括神经保护作用。研究了出生后3至7天大鼠(P3 - P7)的小脑器官型培养物,以检验RU486的神经保护潜力。在这种培养物中,浦肯野细胞会进入凋亡过程,在P3时达到顶峰。本研究表明,RU486(20微摩尔)可保护浦肯野细胞免受此凋亡过程影响。这种神经保护作用既不涉及PR也不涉及GR,因为它不能被这些受体的其他配体模拟或抑制,而且在PR突变小鼠(PR - KO)和脑特异性GR突变小鼠(GRNes/Cre)中仍然发生。强效抗氧化剂不能阻止浦肯野细胞发生这种发育性细胞死亡。在病理性浦肯野细胞死亡中也能观察到RU486的神经保护作用。实际上,这种类固醇能够在遗传性神经退行性共济失调的小鼠模型——浦肯野细胞变性(pcd)突变小鼠的小脑切片器官型培养物中,防止浦肯野细胞死亡。在用RU486处理6天并进一步培养至21天的P0小脑切片中,这种合成类固醇使pcd/pcd浦肯野细胞的存活率提高了16.2倍。我们的结果表明,RU486可能通过一种尚未阐明的新机制来保护浦肯野细胞免于死亡。