摘要
百草枯是一种高效、高毒性的除草剂,急性百草枯中毒主要损伤肺,研究发现细胞凋亡参与百草枯所致的急性肺损伤及肺纤维化的形成。百草枯通过氧化损伤、钙稳态失衡及线粒体损伤诱导肺泡上皮细胞和肺血管内皮细胞凋亡,且通过死亡受体活化途径、线粒体途径、内质网应激途径调控细胞凋亡相关基因的表达。除此之外,百草枯通过激活核转录因子,抑制多型核中性粒细胞(PMN)凋亡,延长PMN生存时间,造成炎性因子大量释放,导致组织细胞损伤。
Paraquat（PQ） is an efficient, highly toxic herbicide, which mainly causes acute lung injury and pulmonary fibrosis. Recent researches have demonstrated that apoptosis participates in the paraquat- induced acute lung injury and pulmonary fibrosis via oxidative damage, disequilibrium of calcium homeostasis and mitochondria damage, as well as regulating the expression of apoptosis-related genes through death recep- tor activation pathway, the mitochondrial pathway and endoplasmic reticulum stress. In addition, paraquat causes massive release of inflammatory cytokines through activation of nuclear transcription factors, inhibition of polymorphonuclear neutrophils （PMN）apoptosis and prolonging PMN survival time, resulting in tissue damage.
出处
《医学综述》
2014年第1期90-92,共3页
Medical Recapitulate
