Isoflurane post-treatment improves pulmonary vascular permeability via upregulation of heme oxygenase-1

Dong, Xiang; Hu, Rong; Sun, Yinghao; Li, Qifang; Hong, Jiang

doi:10.3109/01902148.2013.817627

Cited by 8 publications

(11 citation statements)

References 28 publications

(28 reference statements)

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“…HO-1 has been reported to exert pulmonary protective effects in sepsis. It acts as a potent anti-inflammatory and antioxidant agent through its products carbon monoxide (CO) and biliverdin [ 36 , 37 ]. HO-1 has been reported to prevent ER stress-mediated cell apoptosis in the diabetic model [ 21 , 26 , 27 ].…”

Section: Discussionmentioning

confidence: 99%

“…In the present study, we also found that the HO-1 level increased after ALI. As a potent protective agent of organic injury [ 21 , 26 , 27 , 36 , 37 ], it is unclear whether or not the upregulation of HO-1 is just a simultaneous phenomenon or self-protection mechanism initiation. So, in our study, we pretreated rats which received CLP surgery with hemin (a selective HO-1 inducer) in the absence or presence of ZnPP (HO-1 inhibitor) to explore the role of HO-1 in CLP-induced lung injury.…”

Section: Discussionmentioning

confidence: 99%

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Heme Oxygenase-1 Reduces Sepsis-Induced Endoplasmic Reticulum Stress and Acute Lung Injury

Chen

Wang

Xie

et al. 2018

Mediators of Inflammation

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Background Sepsis leads to severe acute lung injury/acute respiratory distress syndrome (ALI/ARDS) that is associated with enhanced endoplasmic reticulum (ER) stress. Heme oxygenase-1 (HO-1), an ER-anchored protein, exerts antioxidant and protective functions under ALI. However, the role of HO-1 activation in the development of endoplasmic reticulum (ER) stress during sepsis remains unknown. Methods Cecal ligation and puncture (CLP) model was created to induce septic ALI. Lung tissue ER stress was measured 18 hours after CLP. The effects of HO-1 on ER stress during septic ALI were investigated in vivo using HO-1 agonist hemin and antagonist ZnPP. Results Compared with the sham group, ER stress in septic lung increased significantly 18 hours after CLP, which was significantly reduced by pretreatment with the ER inhibitor 4-phenylbutyrate (4-PBA). The lung injury score and the lung wet to dry (W/D) ratio in lungs were significantly reduced in septic rats after ER stress inhibition. Similarly, lung ER stress-related genes' (PERK, eIF2-α, ATF4, and CHOP) levels were attenuated after ER stress inhibition. Furthermore, HO-1 activation by hemin reduced p-PERK, p-eIF2-α, ATF4, and CHOP protein expression and oxidative stress and lung cell apoptosis. Additionally, HO-1 antagonist could aggregate the ER stress-related ALI. Conclusions ER stress was activated during CLP-induced ALI, which may represent a mechanism by which CLP induces ALI. HO-1 activation could inhibit CLP-induced lung ER stress and attenuate CLP-induced ALI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 Reduces Sepsis-Induced Endoplasmic Reticulum Stress and Acute Lung Injury

Chen

Wang

Xie

et al. 2018

Mediators of Inflammation

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“…Isoflurane (ISO) is a widely used inhaled anesthetic with pharmacological properties, such as anti-inflammation, anti-oxidation, and anti-apoptosis [ 19 , 20 ]. ISO protects against lung injury induced by lipopolysaccharides (LPS), zymosan and cecal ligation and puncture [ 19 – 22 ]. Prospects for clinical usage of ISO (1.2%–2.5%) have been hampered due to its adverse systemic effects [ 23 ]; however, our previous studies showed that subanesthetic ISO (0.7%) mitigates zymosan-induced mortality and lung damage in mice by reducing inflammatory responses and reactive oxygen species generation in neutrophils [ 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

“…Prospects for clinical usage of ISO (1.2%–2.5%) have been hampered due to its adverse systemic effects [ 23 ]; however, our previous studies showed that subanesthetic ISO (0.7%) mitigates zymosan-induced mortality and lung damage in mice by reducing inflammatory responses and reactive oxygen species generation in neutrophils [ 24 , 25 ]. Reportedly, ISO post-treatment further enhances zymosan-induced increase in HO-1 expression and activity in mouse lungs and HO-1 elevation and activation improves pulmonary vascular permeability [ 20 , 22 ]. Nevertheless, the role of HO-1 signaling in the protection of AECs-II by ISO remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Epithelial HO-1/STAT3 affords the protection of subanesthetic isoflurane against zymosan-induced lung injury in mice

et al. 2017

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Epithelial dysfunction is a key characteristic of acute lung injury (ALI). Isoflurane (ISO) confers lung protection via anti-inflammatory and anti-apoptotic properties. However, the specific role and potential mechanisms of subanesthetic ISO in lung epithelium protection during zymosan-induced ALI remain unclear. In this study, zymosan increased the expression and activity of beneficial heme oxygenase-1 (HO-1) and signal transducers and activators of transcription 3 (STAT3) in the lung and isolated type II alveolar epithelial cells (AECs-II) from wild-type (WT) mice, which was further enhanced by ISO treatment. ISO reduced the mortality, lung edema, histological changes and pulmonary cell apoptosis, and simultaneously decreased total cells, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels in bronchoalveolar lavage fluid in the zymosan-stimulated WT mice but not in HO-1-deficient mice. Moreover, ISO abated zymosan-augmented lactate dehydrogenase activity, TNF-α and IL-1β production, and apoptosis in WT AECs-II but not in HO-1- or STAT3-silenced cells. Mechanisticly, the epithelial protective effects of ISO on zymosan insult in vivo and in vitro were mediated by a positive feedback loop comprising STAT3 and HO-1. Pro-survival and anti-apoptosis by ISO was highly reliant on activated STAT3, involving in downstream Akt activation and reduced ratio of pro-apoptotic/anti-apoptotic molecules. Overall, HO-1/STAT3 signaling is in favor of lung epithelial protection of ISO in zymosan-challenged mice, suggesting ISO as a valuable therapeutic agent for ALI.

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“…In our previous study, we demonstrated that isoflurane preconditioning resulted in potent pulmonary protection. Posttreatment with isoflurane attenuates ALI by improving vascular permeability through overexpression of HO-1 (24). However, the molecular basis and the anti-inflammatory mechanism of isoflurane effects are still poorly understood.…”

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confidence: 99%

Isoflurane attenuates LPS-induced acute lung injury by targeting miR-155-HIF1-alpha

Zhang

Yang

et al. 2015

Front Biosci

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Isoflurane alleviates the inflammatory response in endotoxin-induced acute lung injury (ALI). In this study, we investigated the protective mechanism of isoflurane postconditioning in lipopolysaccharide (LPS)induced ALI. Exposure to isoflurane decreased miR-155 and upregulated HIF-1 alpha and HO-1 mRNA and protein. The effects of isoflurane on HIF-1 alpha mRNA and protein could be inhibited by overexpression of miR-155. Furthermore, mice overexpressing miR-155 had higher levels of TNF-alpha and IL-1 beta in BALF when exposed to isoflurane after LPS challenge.Conversely, downregulation of miR-155 promoted isoflurane effects on HIF-1 alpha expression. These results suggest that isoflurane posttreatment hr alleviates LPS-induced ALI and cell injury by triggering miR-155-HIF-1 alpha pathway, leading to upregulation of HO-1.

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Isoflurane post-treatment improves pulmonary vascular permeability via upregulation of heme oxygenase-1

Cited by 8 publications

References 28 publications

Heme Oxygenase-1 Reduces Sepsis-Induced Endoplasmic Reticulum Stress and Acute Lung Injury

Heme Oxygenase-1 Reduces Sepsis-Induced Endoplasmic Reticulum Stress and Acute Lung Injury

Epithelial HO-1/STAT3 affords the protection of subanesthetic isoflurane against zymosan-induced lung injury in mice

Isoflurane attenuates LPS-induced acute lung injury by targeting miR-155-HIF1-alpha

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