Inhibition of the complement activation by an adrenal androgen, dehydroepiandrosterone.

T Hidvégi, G K Fehér, T Fehér, E Koó, G Füst
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引用次数: 13

Abstract

The effect of dehydroepiandrosterone (DEA), an adrenal androgen successfully used for preventing attacks in hereditary angioneurotic edema (HANE) patients was studied on the activation of classical and alternative complement pathway. The steroid inhibited both the spontaneous and immune activation of the classical complement pathway (CP), the former effect, however, was found to be more marked than the latter one. DEA exerted its inhibiting effect most probably by interfering with the internal activation of C1. Because DEA rendered HANE patients symptom free but induced only a slight increase in their serum C1-INH level, our present findings suggest that inhibition of CP activation may have a significance in the therapeutic effect of DEA and possibly of other androgens as well.

肾上腺雄激素脱氢表雄酮对补体激活的抑制作用。
研究了脱氢表雄酮(DEA)对遗传性血管神经性水肿(HANE)患者经典补体途径和替代补体途径激活的影响。类固醇对经典补体途径(classic补体pathway, CP)的自发活化和免疫活化均有抑制作用,但前者的作用明显强于后者。DEA的抑制作用很可能是通过干扰C1的内部活化来发挥的。由于DEA使HANE患者无症状,但仅诱导其血清C1-INH水平轻微升高,我们目前的研究结果表明,抑制CP激活可能对DEA和其他雄激素的治疗效果有重要意义。
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