Deletion of apoptosis signal-regulating kinase-1 prevents ventilator-induced lung injury in mice.

摘要: Both hyperoxia and mechanical ventilation can independently cause lung injury. In combination, these insults produce accelerated severe We recently reported that pre-exposure to for 12 hours, followed by with large tidal volumes, induced significant injury epithelial cell apoptosis compared either stimulus alone. also such are inhibited antioxidant treatment. this study, we hypothesized signal–regulating kinase–1 (ASK-1), a redox-sensitive, mitogen-activated protein kinase kinase, plays role in model. To determine the of ASK-1 injury, release inflammatory mediators apoptosis, attributable hours hyperoxia, were volume hyperoxia. Wild-type knockout mice subjected (FiO2 = 0.9) before 4 (tidal 25 μl/g) nonventilated control mice. Lung cytokine measured. The deletion significantly but did not affect mediators, wild-type is an important regulator Further study needed mechanism its downstream lung.