SERPINB1 ameliorates acute lung injury in liver transplantation through ERK1/2-mediated STAT3-dependent HO-1 induction

Yao, Weifeng; Li, Haobo; Luo, Gangjian; Li, Xiang; Chen, Chaojin; Yuan, Ding; Chi, Xinjin; Xia, Zhengyuan

doi:10.1016/j.freeradbiomed.2017.04.011

Cited by 34 publications

(28 citation statements)

References 37 publications

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“…Lung tissues were fixed in 4% formalin and embedded in paraffin as previously described [ 31 ]. 5 μ m lung paraffin sections were dewaxed, hydrated, and then incubated with anti-p-PERK antibody (diluted 1 : 200; Cell Signaling Technology, USA) at 4°C overnight.…”

Section: Methodsmentioning

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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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: Methodsmentioning

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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“…The orthotopic autologous liver transplantation (OALT) model was carried out according to our previous study [ 11 , 12 ]. Rats were randomly divided into six groups ( n = 8) as follows: sham-operated control (sham) and OALT, OALT treated with intralipid (OALT + INT), OALT treated with high dose of propofol (OALT + HPro), OALT treated with low dose of propofol (OALT + LPro), and OALT treated with VAS2870 (OALT + VAS).…”

Section: Methodsmentioning

confidence: 99%

Intravenous Anesthetic Protects Hepatocyte from Reactive Oxygen Species-Induced Cellular Apoptosis during Liver Transplantation In Vivo

Yao

Han

Zhang

et al. 2018

Oxidative Medicine and Cellular Longevity

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Background Liver transplantation leads to liver ischemia/reperfusion (I/R) injury, resulting in early graft dysfunction and failure. Exacerbations of oxidative stress and inflammatory response are key processes in the development of liver I/R injury. Intravenous anesthetic propofol potent effects on free radical scavenging and protects livers against I/R injury. However, the role and mechanism of propofol-mediated hepatic protection in liver transplantation is poorly understood. The aim of this study was to evaluate the role of propofol postconditioning in the liver I/R injury after liver transplantation. Methods Forty-eight rats were randomly divided into six groups: rats receiving either sham operation or orthotopic autologous liver transplantation (OALT) in the absence or presence of propofol (high dose and low dose) postconditioning or intralipid control or VAS2870 (Nox2 special inhibitor). Eight hours after OALT or sham operation, parameters of organ injury, oxidative stress, inflammation, and NADPH-associated proteins were assessed. Results After OALT, severe liver pathological injury was observed that was associated with increases of serum AST and ALT, which were attenuated by propofol postconditioning. In addition, especially high dose of propofol postconditioning reduced TNF-α, IL-1β, IL-6, TLR4, and NF-κB inflammatory pathway, accompanied with decrease of neutrophil elastase activity, MPO activity, 8-isoprotane, p47phox and gp91phox protein expressions, and increase of SOD activity. Inhibition of Nox2 by VAS2870 conferred similar protective effects in liver transplantation. Conclusion Liver transplantation leads to severe inflammation and oxidative stress with NADPH oxidase activation. Propofol postconditioning reduces liver I/R injury after liver transplantation partly via inhibiting NADPH oxidase Nox2 and the subsequent inflammation and oxidative stress.

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“…The activation of MAPK can promote the induction of inflammatory cytokines, COX-2, iNOS and VCAM-1, resulting in up-regulated inflammatory response. Numerous studies have revealed that blocking MAPK activity may be a treatment for ALI/ARDS [ 33 , 34 ].…”

Section: Mechanisms Involved In Ali/ardsmentioning

confidence: 99%

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Zhou

et al. 2021

Pharmacological Research

188

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SERPINB1 ameliorates acute lung injury in liver transplantation through ERK1/2-mediated STAT3-dependent HO-1 induction

Cited by 34 publications

References 37 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

Intravenous Anesthetic Protects Hepatocyte from Reactive Oxygen Species-Induced Cellular Apoptosis during Liver Transplantation In Vivo

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

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