Combined treatment with L-carnitine and a pan-caspase inhibitor effectively reverses amiodarone-induced injury in cultured human lung epithelial cells.

摘要: Amiodarone is an effective class III antiarrhythmic drug, however, the pulmonary toxicity one of most life-threatening complications its use. The present study was designed to determine mechanisms underlying amiodarone. In cultured human lung epithelial cells A549, amiodarone caused cell injury characterized by mitochondrial membrane depolarization, ATP depletion, enhanced propidium iodide (PI) uptake and increase in number Annexin-V positive cells, although population PI-stained appeared earlier not identical that stained suggesting apoptosis necrosis different cells. accompanied with activation caspase-2, -3 -8 but caspase-9, reversed these caspase inhibitors. However, inhibitors had no influence on potential or PI after exposure A549 contrast, cofactors such as L-carnitine acetyl-l-carnitine attenuated abrogated cellular depletion without affecting These finding suggest intracellular events operate cause