妊娠、分娩等腹压增高力学因素是女性盆腔器官脱垂（POP）的主要病因，但其机制尚未阐明。我们的前期研究发现POP患者盆底筋膜组织谷胱甘肽过氧化物酶1（GPx1）表达降低，故推测POP的发生与氧化应激(OS)有关，并在预实验中获得初步证据。本项目对POP和其他良性妇科疾病患者子宫骶韧带成纤维细胞进行原代培养，检测盆底筋膜组织中氧化应激水平及细胞外基质（ECM）的变化；通过四点弯曲细胞力学加载系统模拟盆底力学环境，研究机械力对氧化-抗氧化状态和ECM的影响；比较氧化应激细胞模型和机械力加载模型中ECM的变化，了解机械力是否通过OS途径导致ECM的改变；通过基因沉默或过表达GPx1，研究机械力诱导OS导致ECM的改变在POP发生中的作用。旨在研究机械力、OS、POP三者之间的关系，明确GPx1调控机械力诱导的OS在POP中的作用，从而阐明POP的发生机制，为防治POP提供新的理论基础。

Gestation and delivery can increase intra-abdominal pressure, which is a well-known risk factor for Pelvic Organ Prolapse (POP). But the mechanism remains unclear. Our former findings indicated that the expression of glutathione peroxidase type 1(GPx1) decreased in pelvic floor ligaments from POP patients，suggesting that oxidative stress (OS) may be related with POP, which had been demonstrated in our preliminary experiment. The experiment materials were uterosacral ligament-derived fibroblast from POP or other benign disease patients who received total hysterectomy. First of all, we investigate the changes of extracellular matrix (ECM) and oxidative status of the ligaments from POP patients. Secondly, we set up cytomechanics model to study the changes of ECM, cytoskeleton and oxidative-antioxidant status of the fibroblast under mechanical force. In order to know if the changes of ECM following with OS induced by mechanical force, we will compare the changes of ECM between the cytomechanics model and oxidative stress model. With the gene silence and over expression of GPx1, which regulates the antioxidant defense of the fibroblast, we are going to study the effect of ECM changing caused by OS induced by mechanical force in etiopathogenisis of POP. We also will study the relations among mechanical force, OS and POP, and clarify the role of GPx1 in POP, which GPx1 regulate OS induced mechanical force. This study would explain the mechanisms of POP and provide new theoretical basis for POP prevention and treatment.