在C57BL6小鼠中,双氢睾酮通过激活雄激素受体诱导毛发再生抑制,模拟雄激素性脱发。

PubMed ID
G H
发表日期 2021年May月

原始出处 生物医学和药物治疗=生物医学和药物治疗
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
作者 Fu  Danlan  Huang  Junfei  Li  Kaitao  Chen  Yuxin  He  Ye  Sun  Yang  Guo  Yilong  Du  Lijuan  Qu  Qian  Miao  Yong  Hu  Zhiqi 

文献标题 在C57BL6小鼠中,双氢睾酮通过激活雄激素受体诱导毛发再生抑制,模拟雄激素性脱发。
Dihydrotestosterone-induced hair regrowth inhibition by activating androgen receptor in C57BL6 mice simulates androgenetic alopecia.
Dihydrotestosterone-induced hair regrowth inhibition by activating androgen receptor in C57BL6 mice simulates androgenetic alopecia.

文献摘要

雄激素性脱发(AGA),也称为男性型秃发,是世界范围内最常见的脱发疾病之一。AGA的主要治疗方法包括毛发移植手术、口服药物和LDL激光照射,尽管迄今为止没有任何治疗方法能够完全治愈该疾病。动物模型在探索疾病发展的潜在机制和评估新疗法方面发挥着重要作用。本研究描述了C57BL/6小鼠毛囊中的雄激素受体(AR),其可被双氢睾酮(DHT)激活并转移到细胞核。这导致了在体内和体外设计雄激素诱导的AGA小鼠模型。发现DHT可诱导雄性C57BL/6小鼠早期毛发退化、毛发小型化、毛发密度降低和毛发形态改变。AR拮抗剂比卡鲁胺可部分逆转DHT的这些作用。DHT在脱发的离体模型中也有类似的作用。组织学、器官培养和蛋白质表达的评估可以解释DHT延迟毛发再生的机制。


Androgenic alopecia (AGA), also known as male pattern baldness, is one of the most common hair loss diseases worldwide. The main treatments of AGA include hair transplant surgery, oral medicines, and LDL laser irradiation, although no treatment to date can fully cure this disease. Animal models play important roles in the exploration of potential mechanisms of disease development and in assessing novel treatments. The present study describes androgen receptor (AR) in C57BL/6 mouse hair follicles that can be activated by dihydrotestosterone (DHT) and translocate to the nucleus. This led to the design of a mouse model of androgen-induced AGA in vivo and in vitro. DHT was found to induce early hair regression, hair miniaturization, hair density loss, and changes in hair morphology in male C57BL/6 mice. These effects of DHT could be partly reversed by the AR antagonist bicalutamide. DHT had similar effects in an ex vivo model of hair loss. Evaluation of histology, organ culture, and protein expression could explain the mechanism by which DHT delayed hair regrowth.

Androgenic alopecia (AGA), also known as male pattern baldness, is one of the most common hair loss diseases worldwide. The main treatments of AGA include hair transplant surgery, oral medicines, and LDL laser irradiation, although no treatment to date can fully cure this disease. Animal models play important roles in the exploration of potential mechanisms of disease development and in assessing novel treatments. The present study describes androgen receptor (AR) in C57BL/6 mouse hair follicles that can be activated by dihydrotestosterone (DHT) and translocate to the nucleus. This led to the design of a mouse model of androgen-induced AGA in vivo and in vitro. DHT was found to induce early hair regression, hair miniaturization, hair density loss, and changes in hair morphology in male C57BL/6 mice. These effects of DHT could be partly reversed by the AR antagonist bicalutamide. DHT had similar effects in an ex vivo model of hair loss. Evaluation of histology, organ culture, and protein expression could explain the mechanism by which DHT delayed hair regrowth.


获取全文 10.1016/j.biopha.2021.111247