KNDy神经元在绝经后期妇女血管舒缩症状病理机制中的作用*

Pathological mechanism of KNDy neurons in postmenopausal women with vasomotor symptoms*

摘要:

血管舒缩症状（VMS）困扰着近80%的绝经后期妇女，但是对VMS病因的了解十分有限。与生殖轴相关的神经内分泌回路在绝经后期发生显著变化。目前很多研究发现在绝经后期由于缺乏卵巢类固醇激素负反馈，女性下丘脑的KNDy神经元的形态及神经肽基因表达发生改变，因此推测KNDy神经元可能在VMS病理机制中发挥作用。在大鼠模型中，通过KNDy神经元的消融可以减少尾部皮肤血管舒张，部分阻断雌激素对温度调节的影响。此外，KNDy神经元可以通过中位视前核（MnPO）中的神经激肽B（NKB）信号影响大鼠尾部皮肤血管舒张。该文对调节KNDy神经元可能成为治疗VMS的新方法作一综述。

Abstract:

Despite affecting nearly 80% of menopausal women, the etiology of vasomotor symptoms (VMS) remains unknown. The neuroendocrine circuit associated with the reproductive axis has undergone significant changes after menopause. Many studies have shown that the absence of negative feedback of steroid hormones which synthesized in postmenopausal ovary causes changes in neuropeptide gene expression and kisspeptin/neurokinin B/dynorphin (KNDy) neurons morphology in the hypothalamus of women. Therefore, it is possible that KNDy neurons have an important influence on the mechanism of VMS. In the rat models, the ablation of KNDy neurons can reduce the cutaneous vasodilation of the rat’s tail and partially block the effects of estrogen on thermoregulation. In addition, KNDy neurons can modulate the cutaneous vasodilation of rats through neurokinin B (NKB) signaling in the median preoptic nucleus (MnPO). These studies suggest that the regulation of KNDy neurons may be a promising treatment for VMS. In this paper, we review the possibility of regulating kndy neurons as a new therapy for VMS.