女性性唤起功能障碍发病机制的研究

女性性功能障碍是一种发病率高却未被重视的疾病，其中性唤起功能障碍是其主要表现，相应的基础和临床研究显著滞后于男性，严重影响女性健康和社会稳定。性唤起时阴道平滑肌细胞是神经内分泌网络调节的最终效应单位。本研究通过对比性功能障碍者和对照组阴道壁新鲜标本的组织学和生物力学状态以及平滑肌细胞内一氧化氮（NO）-cGMP和血管活性肠肽（VIP）-cAMP相关信号通路上分子的表达差异，分别在器官和分子水平解释性唤起功能障碍的发病机制，为临床诊治提供依据，并探讨雌激素与NO、VIP对阴道平滑肌细胞功能的影响及相互作用，分析不同信号途径的作用机制，为进一步的体内研究和药物研发提供基础。既往对性唤起功能障碍的研究多基于动物模型，本研究以平滑肌细胞为靶点，以相关信号通路为切入点,为人类自身的组织力学及分子生物学研究，国内外罕见，具有较高的学术价值及巨大的社会和经济效益。

Female sexual arousal disorder (FSAD) is a major component of female sexual dysfunction (FSD) which is widespread in society and is highly associated with impaired quality of life. Etiologic mechanisms of FSAD are poorly understood and literature is scarce. It's a fact that vaginal smooth muscle relaxation is the necessary result of neuroendocrine network regulation. We can illustrate the etiologic mechanisms of FSAD by research focused on differences on histomorphology and biomechanics of the vaginal tissues as well as nitric oxide (NO)/cGMP and vasoactive intestinal polypeptide (VIP)/ cGAP signaling pathway in vaginal smooth muscle cells between FSAD patients and the controls. We also study the impact of estrogen and neurotransmitters such as NO and VIP on the function of vaginal smooth muscle and the relationship between them. Previous researches conducted on FSD were mainly on animal models which were controversy. The present study investigate the biomechanics of the human vaginal smooth muscle and the signaling pathway in the smooth muscle cells to explore the etiologic mechanisms of FSAD so as to provide basis for future research and pharmaceutical treatment.