摘要
百草枯（PQ）中毒可引起肺损伤,导致肺水肿、肺泡出血和肺纤维化.细胞外基质（ECM）构成正常肺组织骨架,保持肺组织结构的完整性,并能维持肺上皮细胞及内皮细胞的生理功能.基质金属蛋白酶（MMPs）是体内重要的水解酶,几乎能降解所有的ECM,但其活性可被其特异性抑制剂--基质金属蛋白酶组织抑制剂（TIMPs）所抑制.近年来许多研究发现,PQ中毒后,MMPs与TIMPs在肺泡损伤、肺组织异常重塑和肺纤维化的发生、发展过程中存在动态变化.PQ中毒引发的肺损伤可能与MMPs与TIMPs之间失衡导致的ECM反复破坏、修复、重构与过度沉积有关.本文就ECM与MMPs/TIMPs在PQ中毒致肺损伤机制中的作用做一综述.
Objective Paraquat （PQ） poisoning can cause lung injury, resulting in pulmonary edema, alveolar hemorrhage and pulmonary fibrosis. Extracellular matrix （ECM） , which constitutes the skeleton and keeps structure integrity of normal lung tissues, can also maintain the physiological function of lung epithelial cells and endothelial cells. Matrix metalloproteinases （MMPs） are important hydrolytic enzymes in the body, and degrade almost all of the ECM, but the activity can be inhibited by their specific inhibitors - tissue inhibitors of metalloproteinases （TIMPs）. Recent studies have found that MMPs and TIMPs are dynamically changed in alveolar injury, abnormal lung tissue remodeling and pulmonary fibrosis induced by PQ poisoning. The PQ - induced lung injury may relate with repeated destruction, repair, reconstruction and excessive deposition of ECM caused by the imbalance of MMPs and TIMPs. In this paper, the roles of ECM and MMPs/TIMPs are reviewed based on the mechanism of lung injury induced by PQ poisoning.
出处
《中国急救医学》
CAS
CSCD
北大核心
2013年第10期882-885,共4页
Chinese Journal of Critical Care Medicine
