The journal of trauma and acute care surgery · 2014
Improvement of ventilation-induced lung injury in a rodent model by inhibition of inhibitory κB kinase.
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Shu Yu-Sheng, Tao Wei, Miao Qian-Bing, Zhu Ya-Bing, Yang Yi-Feng
Аннотация
BACKGROUND: Inhibition of nuclear factor κB (NF-κB) activation is a well-know strategy to ameliorate ventilation-induced lung injury (VILI). Inhibitory κB kinase (IKK) plays a key role in the regulation of NF-κB activation. In this study, we determined whether inhibition of IKK by an IKK inhibitor exerts lung protection in a rat model of VILI.
METHODS: Anesthetized and mechanically ventilated Sprague-Dawley rats were randomly assigned to a standard (tidal volume, 8 mL/kg) or high-tidal volume (tidal volume, 25 mL/kg) ventilation group. An IKK inhibitor (IKK 16) or vehicle was administrated 1 hour before the induction of VILI. All groups were ventilated and observed for 5 hours.
RESULTS: High-pressure ventilation caused activation of NF-κB, increased pulmonary inflammatory mediator levels, lung edema, and impairment of gas exchange. The IKK inhibitor treatment significantly reduced these changes and increased interleukin 10 levels, heme oxygenase 1 activity, protein kinase B (Akt) phosphorylation levels, and nuclear amounts of nuclear factor E2-related factor 2 protein.
CONCLUSION: IKK may be a therapeutic target for VILI. An IKK inhibitor, IKK 16, can dampen VILI in rats. The beneficial effect of the IKK 16 may be mediated through the inhibition of NF-κB pathway and up-regulation of nuclear factor E2-related factor 2-regulated heme oxygenase 1 through the activation of the phosphatidylinositol 3 kinase/Akt.
METHODS: Anesthetized and mechanically ventilated Sprague-Dawley rats were randomly assigned to a standard (tidal volume, 8 mL/kg) or high-tidal volume (tidal volume, 25 mL/kg) ventilation group. An IKK inhibitor (IKK 16) or vehicle was administrated 1 hour before the induction of VILI. All groups were ventilated and observed for 5 hours.
RESULTS: High-pressure ventilation caused activation of NF-κB, increased pulmonary inflammatory mediator levels, lung edema, and impairment of gas exchange. The IKK inhibitor treatment significantly reduced these changes and increased interleukin 10 levels, heme oxygenase 1 activity, protein kinase B (Akt) phosphorylation levels, and nuclear amounts of nuclear factor E2-related factor 2 protein.
CONCLUSION: IKK may be a therapeutic target for VILI. An IKK inhibitor, IKK 16, can dampen VILI in rats. The beneficial effect of the IKK 16 may be mediated through the inhibition of NF-κB pathway and up-regulation of nuclear factor E2-related factor 2-regulated heme oxygenase 1 through the activation of the phosphatidylinositol 3 kinase/Akt.