百草枯中毒致肺损伤分子机制的研究进展

Advances in molecular mechanism of lung injury induced by paraquat poisoning

百草枯是一种联吡啶二氯化物非选择性除草剂,上世纪风靡全球。因中毒死亡率极高且没有特效解毒药物而被大多数国家禁止使用,但其中毒死亡病例仍时常发生,因此对百草枯中毒的分子机制和解毒药物研究具有重要的临床意义。百草枯中毒引起肺、肝、肾、心、脑等多脏器功能障碍;分子机制复杂,有过度炎症反应学说、氧化还原反应失衡、氧化应激自由基损伤、钙超载、NO分子损伤、细胞凋亡等。针对百草枯中毒的治疗,近几年新研发的有百草枯抗体、通路靶点阻断剂及相关因子抗体应用等,虽然取得了一定效果,但救治有效率没有明显改善。本文就百草枯中毒致肺损伤涉及信号传导通路的机制进行总结,旨在为进一步研究提供理论基础。

Paraquat is a bipyridine dichloride non-selective herbicide,which was widely used in the world in the last century.Now,paraquat is banned in most countries because of the extremely high lethality and the lack of specific detoxification drugs.However,death due to paraquat poisoning still occurs frequently,thus it is of great clinical significance to explore the molecular mechanism of paraquat poisoning and the detoxification drugs.Paraquat poisoning causes multiple dysfunction of the lung,liver,kidney,heart,and brain through complex molecular mechanisms.About the mechanism there are excessive inflammatory reaction theory,REDOX reaction imbalance theory,oxidative stress free radical damage theory,calcium overload theory,NO molecular damage and cell apoptosis theory,etc.For the treatment of paraquat poisoning,paraquat antibody,pathway target blocker and related factor antibody have been developed in recent years.Although certain effects have been achieved,the treatment efficiency has not been significantly improved.This paper summarized the mechanism of signal transduction pathways involved in lung injury induced by paraquat poisoning in order to provide a theoretical basis for further research.