Protective Effects of Idebenone against Sepsis Induced Acute Lung Damage

Akpınar, Erol; Kutlu, Zerrin; Köse, Duygu; Aydin, Pelin; Tavacı, Taha; Bayraktutan, Zafer; Yüksel, Tuğba; Yıldırım, Serkan; Eser, Gizem; Dinçer, Büşra

doi:10.1080/08941939.2021.1898063

Cited by 16 publications

(9 citation statements)

References 46 publications

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“…The discovery of precise and effective target inhibitors still depends on the study of genes and proteins involved in the pathway, but the study of diagnostic genes and proteomics of inflammatory diseases is still at a preliminary stage. Therefore, ALI induced by more surgical critical care conditions needs to be more thoroughly explored, especially in ischemia/reperfusion [ 70 , 71 ], sepsis [ 72 ], trauma [ 73 ], and transfusion [ 74 , 75 ]. In the future, we plan to analyze the interaction between various proteins and genes to deepen our understanding of the mechanism of inflammatory diseases and provide for effective diagnosis and treatments.…”

Section: Discussionmentioning

confidence: 99%

Signal Pathways and Markers Involved in Acute Lung Injury Induced by Acute Pancreatitis

Zhou

Wang

2021

Disease Markers

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Acute pancreatitis (AP) is a common acute abdominal disease with a mortality rate of about 30%. Acute lung injury (ALI) is a common systemic complication of acute pancreatitis, with progressive hypoxemia and respiratory distress as the main manifestations, which can develop into acute respiratory distress syndrome or even multiple organ dysfunction syndrome (MODS) in severe cases, endangering human health. In the model of AP, pathophysiological process of the lung can be summarized as oxidative stress injury, inflammatory factor infiltration, and alveolar cell apoptosis. However, the intrinsic mechanisms underlying AP and how it leads to ALI are not fully understood. In this paper, we summarize recent articles related to AP leading to ALI, including the signal transduction pathways and biomarkers of AP-ALI. There are factors or pathway aggravating ALI, the JAK2-STAT3 signaling pathway, NLRP3/NF-κB pathway, mitogen-activated protein kinase, PKC pathway, neutrophil protease (NP)-LAMC2-neutrophil pathway, and the P2X7 pathway, and there are important transcription factors in the NRF2 signal transduction pathway which could give researchers better understanding of the underlying mechanisms controlling AP and ALI and lay the foundation for finally curing ALI induced by AP.

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Section: Discussionmentioning

confidence: 99%

Signal Pathways and Markers Involved in Acute Lung Injury Induced by Acute Pancreatitis

Zhou

Wang

2021

Disease Markers

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“…All rats were fed a standard pellet diet and water ad libitum . Varying concentrations of IDE were applied for the administration of rats ( 12 ). All rats were randomly separated into five groups (n=5): control group, sepsis group, sepsis + IDE 50 mg/kg group, sepsis + IDE 100 mg/kg group, and sepsis + IDE 200 mg/kg group.…”

Section: Methodsmentioning

confidence: 99%

“…Qian et al proposed that IDE could attenuate oxidative stress and neuroinflammation in rats with vascular dementia, which indicated the therapeutic potential of IDE for vascular dementia ( 11 ). Interestingly, IDE has also been found to protect against sepsis-induced lung damage ( 12 ). Nevertheless, whether IDE can alleviate sepsis-induced liver injury remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Idebenone reduces sepsis-induced oxidative stress and apoptosis in hepatocytes via RAGE/p38 signaling

Gou¹,

Jin²,

Xia³

2022

Ann Transl Med

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Background: Sepsis-induced liver dysfunction is believed to be an independent risk factor for multiple organ dysfunction and death. Idebenone (IDE), a synthetic analog of coenzyme Q10 (CoQ10), possesses an antioxidizing property. The present study aimed to investigate the efficacy of IDE on sepsis-induced liver injury and discuss its reaction mechanism in vivo and in vitro. Methods:To establish an in vivo model of sepsis-induced liver injury, rats were treated with highgrade cecal ligation and puncture (CLP). Hematoxylin-eosin staining was applied to observe the liver pathological changes, and liver function was examined using alanine aminotransferase (ALT) and aspartate aminotransferase (AST) assay kits. Enzyme-linked immunosorbent assay (ELISA) kits were employed to assess the levels of inflammatory cytokines in serum and tissues. The activities of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were analyzed using MDA, SOD, and GSH-Px assay kits, respectively. The apoptosis of liver tissues was measured by terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) staining, and western blot was employed to estimate apoptosis-related proteins. In vitro, 0.5 μg/mL lipopolysaccharide (LPS) was adopted to administrate primary hepatocytes. The expressions of receptor for advanced glycation end products (RAGE)/p38-related proteins were evaluated by western blot. Cell counting kit-8 (CCK-8) and dichloro-dihydro-fluorescein diacetate (DCFH-DA) assays were utilized to estimate cell viability and reactive oxygen species (ROS) content.Moreover, the transfection efficacy of overexpression (Ov)-RAGE in primary hepatocytes was tested by realtime quantitative polymerase chain reaction (RT-qPCR) and western blot.Results: IDE could improve liver function and reduce sepsis-induced pathological damage. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the serum and liver tissue of sepsis rats were suppressed by IDE. Additionally, IDE repressed the oxidative stress and apoptosis of liver tissues in sepsis-induced rats. IDE also inhibited RAGE/p38 signaling. Furthermore, IDE revived the decreased viability in LPS-induced hepatocytes concentration-dependently. After overexpressing RAGE, RAGE expression in hepatocytes was significantly elevated. Further functional experiments revealed that IDE attenuated cell viability injury, apoptosis, oxidative stress, and inflammatory damage in LPS-induced hepatocytes via RAGE/p38 signaling.Conclusions: IDE helped to protect against sepsis-induced liver injury via the regulation of RAGE/p38 signaling.

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“…In their study, pulmonary static inflation with 50% Xenon during CPB can triggered anti-inflammatory responses and suppressed pro-inflammatory and oxidative effects. In another sepsis-induced ALI model, the antioxidant idebenone (IDE) alleviated inflammatory response by reducing free radicals and lipid peroxidation [ 91 ]. Escitalopram is clinically used as an antidepressant drug and can inhibit lung inflammation through the SIK2/HDAC4/NF-kB pathway [ 92 ].…”

Section: Drug Therapymentioning

confidence: 99%

Acute Lung Injury in aortic dissection : new insights in anesthetic management strategies

Yang

2023

J Cardiothorac Surg

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Acute aortic dissection (AAD) is a severe cardiovascular disease characterized by rapid progress and a high mortality rate. The incidence of acute aortic dissection is approximately 5 to 30 per 1 million people worldwide. In clinical practice, about 35% of AAD patients are complicated with acute lung injury (ALI). AAD complicated with ALI can seriously affect patients’ prognosis and even increase mortality. However, the pathogenesis of AAD combined with ALI remains largely unknown. Given the public health burden of AAD combined with ALI, we reviewed the anesthetic management advances and highlighted potential areas for clinical practice.

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Protective Effects of Idebenone against Sepsis Induced Acute Lung Damage

Cited by 16 publications

References 46 publications

Signal Pathways and Markers Involved in Acute Lung Injury Induced by Acute Pancreatitis

Signal Pathways and Markers Involved in Acute Lung Injury Induced by Acute Pancreatitis

Idebenone reduces sepsis-induced oxidative stress and apoptosis in hepatocytes via RAGE/p38 signaling

Acute Lung Injury in aortic dissection : new insights in anesthetic management strategies

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