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Suppression of Endoplasmic Reticulum Stress Attenuates Hyperoxia-Induced Acute Lung Injury
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A2975 - Suppression of Endoplasmic Reticulum Stress Attenuates Hyperoxia-Induced Acute Lung Injury
Author Block: H. P. Pao1, K. L. Huang2, S. J. Chu2; 1Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei City, Taiwan, 2Medicine, Tri-Service General Hospital, Taipei City, Taiwan.
Administration of high concentrations of inspired oxygen is common as a life-saving therapy for patients with cardiorespiratory diseases. Unfortunately, the toxicity generated by prolonged hyperoxia may cause acute lung injury (ALI) and acute respiratory distress syndrome, multiple organ failure and eventually death. Endoplasmic reticulum (ER) stress that disrupts ER function can occur in response to a wide variety of cellular stressors that lead to the accumulation of unfolded and misfolded proteins in the ER. Many studies had showed that ER stress amplified inflammatory reactions and involved in various inflammatory diseases. However, little is known regarding the role of ER stress in hyperoxia-induced lung inflammation. In this study, we investigated the influence of ER stress inhibitor, 4-phenyl butyric acid (4-PBA), in hyperoxia-induced ALI in mice. Treatment with 4-PBA in the hyperoxia groups significantly prolonged the survival of mice, decreased lung edema and lung injury scores, reduced the increased levels of tumor necrosis factor-alpha, interleukin 6, macrophage inflammatory protein 2, lactate dehydrogenase ,and protein in bronchoalveolar lavage fluid when compared with the PBS-treated groups. In addition, 4-PBA reduced the expression of CCAAT-enhancer-binding protein homologous protein (CHOP) protein in the lung tissue. In vitro study, 4-PBA also attenusted hyperoxia-induced barrier dysfunction on mouse lung epithelial cells (MLE-12). These results suggested that 4-PBA protected against hyperoxia-induced ALI in mice.
Author Block: H. P. Pao1, K. L. Huang2, S. J. Chu2; 1Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei City, Taiwan, 2Medicine, Tri-Service General Hospital, Taipei City, Taiwan.
Administration of high concentrations of inspired oxygen is common as a life-saving therapy for patients with cardiorespiratory diseases. Unfortunately, the toxicity generated by prolonged hyperoxia may cause acute lung injury (ALI) and acute respiratory distress syndrome, multiple organ failure and eventually death. Endoplasmic reticulum (ER) stress that disrupts ER function can occur in response to a wide variety of cellular stressors that lead to the accumulation of unfolded and misfolded proteins in the ER. Many studies had showed that ER stress amplified inflammatory reactions and involved in various inflammatory diseases. However, little is known regarding the role of ER stress in hyperoxia-induced lung inflammation. In this study, we investigated the influence of ER stress inhibitor, 4-phenyl butyric acid (4-PBA), in hyperoxia-induced ALI in mice. Treatment with 4-PBA in the hyperoxia groups significantly prolonged the survival of mice, decreased lung edema and lung injury scores, reduced the increased levels of tumor necrosis factor-alpha, interleukin 6, macrophage inflammatory protein 2, lactate dehydrogenase ,and protein in bronchoalveolar lavage fluid when compared with the PBS-treated groups. In addition, 4-PBA reduced the expression of CCAAT-enhancer-binding protein homologous protein (CHOP) protein in the lung tissue. In vitro study, 4-PBA also attenusted hyperoxia-induced barrier dysfunction on mouse lung epithelial cells (MLE-12). These results suggested that 4-PBA protected against hyperoxia-induced ALI in mice.
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