摘要
炎症是临床上常见而又重要的基本病理过程。过度的炎症反应对组织器官有着巨大的损伤作用。一氧化碳是一种小分子气体，在体内主要由血红素氧合酶降解血红素而生成，它的多种生物学活性均与其细胞保护功能有关，如抗炎、抗凋亡、抗增殖及舒张血管。基础研究发现：在多种炎症模型中，一氧化碳均具有良好的抗炎效应，其作用的主要细胞细胞信号通路包括丝裂原活化蛋白激酶信号通路、Toll样受体信号通路、核转录因子-κB信号通路、Janus激酶-信号传导和转录激活子信号通路等。临床研究中，一氧化碳并未取得良好的保护效果。该文探讨一氧化碳的抗炎作用机制，以期为更进一步研究提供理论参考。
Inflammation is a common and important clinical basic pathological process, and excessive inflammatory response has tremendous damage to tissues and organs. Carbon monoxide is a kind of small-molec- ular gas, which is generated by degradation of heine in the body. It has been demonstrated that endogenous car- bon monoxide has a variety of biological activities involved in its cytoprotective efects, such as anti-inflammation, anti-apoptosis, anti-proliferation and vasodilation. Carbon monoxide has good anti-inflammatory effect in a variety of inflammatory models in basic research, which play roles in following main cell signal pathways include mitogen-activated potein kinase（ MAPK ） signal pathway ,toll-like receptor（TLR） signal pathway ,nuclear factor KappaB（NF-κB） signal pathway,janus kinase-signal transducer and activator of transcription（JAK-STAT） sig- nal pathway. Unfortunately, carbon monoxide did not show good protective effect in clinical research. This re- view summarizes the anti-inflammatory mechanism of carbon monoxide, so as to provide theoretical reference for further study.
出处
《国际儿科学杂志》
2015年第5期538-541,共4页
International Journal of Pediatrics
