Influence of estrogens on the androgen metabolism in different subunits of human hair follicles.
Influence of estrogens on the androgen metabolism in different subunits of human hair follicles.
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雌激素对人毛囊不同亚基雄激素代谢的影响。
DOI：
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发表时间：
2001
期刊：
影响因子：
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通讯作者：
R. Hoffmann
中科院分区：
文献类型：
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作者：
S. Niiyama;R. Happle;R. Hoffmann
雌激素介导的雄激素性脱发诱导毛发生长的分子途径尚不清楚。一些作者发现雌二醇(E)抑制5α -还原酶（5α -r）活性，因此我们解决了17α -或17β -E是否能够调节人类毛囊分离腔室中5α -r、3β -羟基类固醇脱氢酶（3β - hsd）或17β -羟基类固醇脱氢酶（17β - hsd）活性的问题。为此，对志愿者进行头皮活检，并从每个活检组织中剥离根鞘、结缔组织鞘和真皮乳头（DP），并在3h -睾酮(T)存在下孵育48小时，此外，还有17α - e、17β - e、黄体酮或非那雄胺。然后对培养上清进行高效液相色谱分析，检测t代谢物。在测试浓度下，非那雄胺被发现是双氢睾酮（DHT）形成的主要抑制剂。即使是1nm的非那雄胺也能抑制DHT合成86%，1nm的黄体酮能抑制75%。雌激素对DP中DHT合成的抑制作用较弱（例如，100 nM 17α - e: 20%; 100 nM 17β - e: 60%）。E是否直接抑制DP中的5 α - r，或者雌激素的作用是否可以解释为T向较弱的雄激素(如雄烯二酮（通过17 - β - hsd），雄烯二醇（通过3 - β - hsd）或17 - β -E（通过芳香化酶）的转化增加，从而减少了可用于转化为DHT的T的量，仍有待证明。
The molecular pathways involved in estrogen-mediated induction of hair growth in androgenetic alopecia are unknown. Some authors found that estradiol (E) inhibited 5alpha-reductase (5alpha-R) activity and therefore we addressed the question whether 17alpha- or 17beta-E are able to modulate the activity of 5alpha-R, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) or 17beta-hydroxysteroid dehydrogenase (17beta-HSD) in isolated compartments of human hair follicles. For this purpose, scalp biopsies from volunteers were taken and from each biopsy root sheaths, connective tissue sheaths and dermal papillae (DP) were dissected and incubated in the presence of 3H-testosterone (T) and, in addition, either 17alpha-E, 17beta-E, progesterone or finasteride for up to 48 hrs. Thereafter high-performance liquid chromatography analysis of culture supernatants was performed to detect T-metabolites. At the tested concentrations, finasteride was found to be a major inhibitor of dihydrotestosterone (DHT) formation. Even 1 nM finasteride inhibited DHT synthesis in DP by 86% and 1 nM progesterone by 75%. Estrogens were less able to inhibit the synthesis of DHT in DP (e.g. 100 nM 17alpha-E: 20%; 100 nM 17beta-E: 60%). Whether E directly inhibits 5alpha-R in DP's or whether the effect of estrogens might be explained by an increased conversion of T to the weaker androgens such as androstendione (via 17beta-HSD), androstenediol (via 3beta-HSD) or 17beta-E (via aromatase), thereby diminishing the amount of T available for the conversion to DHT, remains to be shown.