探讨PM2.5暴露的肺外毒理效应对绝经后骨代谢的影响机制

骨代谢是骨吸收和骨形成两方面动态过程,其分子机制涉及氧化应激、炎症因子、雌激素及相关受体(如AhR)等多种因素、多途径调节,在骨重塑方面起到至关重要的作用。大气细颗粒物(airborne particulate matter,PM2.5)因其粒径小、表面积大、活性强,是有毒、有害物质吸附在其表面的有效载体,且气溶胶在大气中的沉降速率低、搬运距离远,对人体危害更大。PM2.5可随呼吸道于肺泡中聚集,破坏肺泡毛细血管屏障而进入循坏系统作用于全身各个脏器,造成各个脏器不同程度受损,并激活一系列全身的或局部的炎性因子、氧化作用和相关受体(如AhR)等对成骨细胞及破骨细胞的分化增殖起到调控作用,参与骨代谢。

To explore the mechanism of extrapulmonary toxicological effects of PM2.5 exposure on postmenopausal bone metabolism

Bone metabolism is a dynamic process of bone resorption and bone formation. Its molecular mechanism involves oxidative stress, inflammatory factors, estrogen and related receptors (such as AhR). It plays an important role in bone remodeling. Atmospheric fine particulate matter (airborne particulate matter, PM2.5) because of its small particle size, large surface area and strong activity, is an effective carrier for toxic and harmful substances adsorbed on its surface, and the deposition rate of aerosols in the atmosphere is low and the transport distance is long, so it is more harmful to human beings. PM2.5 can accumulate in the alveoli of respiratory tract, destroy the alveolar capillary barrier and enter the blood system to act on all organs of the whole body, resulting in different degrees of damage to each organ, and activating a series of systemic or local inflammatory factors, oxidation and related receptors (such as AhR), which regulate the differentiation and proliferation of osteoblasts and osteoclasts and participate in bone metabolism.