Autophagic Cell Death and Apoptosis Jointly Mediate Cisatracurium Besylate-Induced Cell Injury

摘要: Cisatracurium besylate is an ideal non-depolarizing muscle relaxant which widely used in clinical application. However, some studies have suggested that cisatracurium can affect cell proliferation. Moreover, its specific mechanism of action remains unclear. Here, we found the number GFP-LC3 (green fluoresent protein-light chain 3) positive autophagosomes and rate mitochondria fracture both increased significantly drug-treated MitoDsRed stable HeLa cells. promoted co-localization LC3 induced formation autolysosomes. Levels mitochondrial proteins decreased, were reversed by lysosome inhibitor Bafinomycin A1. Similar results with evidence dose-dependent effects Human Umbilical Vein Endothelial Cells (HUVECs). lowered HUVEC viability to 0.16 (OD490) at 100 µM 0.05 after 48 h vitro; it death 56% 60% 24 a concentration- time-dependent manner (p < 0.01). Cell proliferation decreased four fold Atg5 WT (wildtype) MEF (mouse embryonic fibroblast) 0.01) but was unaffected KO (Knockout) MEF, even upon treatment high dose cisatracurium. significant increase wild-type MEFs presence apoptosis zVAD. Thus, conclude activation autophagic pathways contributes cisatracurium-mediated injury.