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首页> 外文期刊>Life sciences >Oxidized glucocorticoids counteract glucocorticoid-induced apoptosis in murine thymocytes in vitro
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Oxidized glucocorticoids counteract glucocorticoid-induced apoptosis in murine thymocytes in vitro

机译：氧化的糖皮质激素抵消了糖皮质激素诱导的小鼠胸腺细胞凋亡

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摘要

11 beta -hydroxyglucocorticoids (HGCs) are known to induce apoptosis in immature T cells. Here we show that 11-oxoglucocorticoids (OGCs), which are oxidized metabolites of HGCs, counteract the apoptosis-inducing effects of HGC in murine thymocytes in vitro. Corticosterone at concentrations ranging from 0.1-100 muM induced apoptosis in thymocytes obtained from C57BL/6J mice aged 4 weeks, as demonstrated by cell staining with anti-phosphatidylserine antibody, a decrease in mitochondrial membrane potential, and DNA fragmentation. Go-culture of the cells with 10-100 muM of OGCs, dehydrocorticosterone, cortisone, and prednisone significantly inhibited thymocyte apoptosis induced by 1 muM corticosterone, (p<0.006). Among the other 6 physiological metabolites of the HGCs we tested, 20-dehydrocortisol also showed considerable inhibitory effect on corticosterone-induced thymocyte apoptosis. Corticosterone-treatment of thymocytes in vitro decreased the number of CD4 and CD8 double positive cells, while co-culturing the cells with dehydrocorticosterone significantly attenuated this corticosterone effect (p<0.0001). Numbers of double-negative cells and single-positive cells were not significantly affected by corticosterone, dehydrocorticosterone, or both together. These results raised the possibility that OGCs and probably other HGC metabolites can regulate apoptotic cell death of immature double-positive thymocytes induced by HGC. (C) 2001 Elsevier Science Inc. All rights reserved. [References: 23]
机译：已知11种β-羟基糖皮质激素（HGC）可以诱导未成熟T细胞凋亡。在这里，我们显示11-氧糖皮质激素（OGCs），这是HGCs的氧化代谢产物，抵消了HGC在体外对小鼠胸腺细胞的凋亡诱导作用。如用抗磷脂酰丝氨酸抗体对细胞染色，线粒体膜电位降低和DNA片段化所证实，浓度为0.1-100μM的皮质酮可诱导4周龄C57BL / 6J小鼠的胸腺细胞凋亡。用10-100μM的OGC，脱氢皮质酮，可的松和泼尼松对细胞进行去培养，可显着抑制1μM皮质酮诱导的胸腺细胞凋亡（p <0.006）。在我们测试的HGC的其他6种生理代谢产物中，20α-脱氢皮质醇也显示出对皮质酮诱导的胸腺细胞凋亡的显着抑制作用。体外对胸腺细胞进行皮质酮处理可减少CD4和CD8双阳性细胞的数量，而将细胞与脱氢皮质酮共同培养可显着减弱这种皮质酮作用（p <0.0001）。皮质酮，脱氢皮质酮或两者并没有显着影响双阴性细胞和单阳性细胞的数量。这些结果增加了OGC和其他HGC代谢物可以调节HGC诱导的未成熟双阳性胸腺细胞凋亡的可能性。 （C）2001 Elsevier Science Inc.保留所有权利。 [参考：23]

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