Short-term administration of (-)-epigallocatechin gallate reduces hepatic steatosis and protects against warm hepatic ischemia/reperfusion injury in steatotic mice

2005 ◽  
Vol 11 (3) ◽  
pp. 298-308 ◽  
Author(s):  
Ryan N. Fiorini ◽  
Jennifer L. Donovan ◽  
David Rodwell ◽  
Zachary Evans ◽  
Gang Cheng ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Hepatic Steatosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Epigallocatechin Gallate ◽  
Short Term ◽  
Hepatic Ischemia ◽  
Term Administration ◽  
Hepatic Ischemia Reperfusion

scholarly journals The Impact of Hepatic Steatosis on Hepatic Ischemia-Reperfusion Injury in Experimental Studies: A Systematic Review

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Michael J. J. Chu ◽  
Anthony J. R. Hickey ◽  
Anthony R. J. Phillips ◽  
Adam S. J. R. Bartlett
Keyword(s):  
Systematic Review ◽  
Reperfusion Injury ◽  
Hepatic Steatosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Experimental Studies ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
The Impact ◽  
Macrovesicular Steatosis

Background. The impact of hepatic steatosis on outcome following hepatic ischemia-reperfusion injury (IRI) remains controversial with conflicting clinical results. A number of experimental studies have been published examining the relationship between hepatic steatosis and IRI. This systematic review evaluates these experimental studies.Methods. An electronic search of the Medline and Embase databases (January 1946 to June 2012) was performed to identify studies that reported relevant outcomes in animal models of hepatic steatosis subjected to IRI.Results. A total of 1314 articles were identified, of which 33 met the predefined criteria and were included in the study. There was large variation in the type of animal model, duration, and type of IRI and reporting of histological findings. Increased macrovesicular steatosis (>30%) was associated with increased histological damage, liver function derangement, and reduced survival. Increased duration of warm or cold ischemia had a negative impact on all outcomes measured. Microvesicular steatosis did not influence outcome.Conclusions. Findings from this systemic review support the hypothesis that livers with >30% macrovesicular steatosis are less tolerant of IRI. Clinically, it is likely that these findings are applicable to patients undergoing hepatic resection, but further studies are required to confirm these data.

scholarly journals Ischemia/Reperfusion Injury of Fatty Liver Is Protected by A2AR and Exacerbated by A1R Stimulation through Opposite Effects on ASK1 Activation

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3171
Author(s):  
Elisa Alchera ◽  
Bangalore R. Chandrashekar ◽  
Nausicaa Clemente ◽  
Ester Borroni ◽  
Renzo Boldorini ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Reperfusion Injury ◽  
Hepatic Steatosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Dependent Inhibition ◽  
Effective Therapeutic Strategy ◽  
Hepatic Ischemia Reperfusion

Hepatic ischemia/reperfusion injury (IRI) is aggravated by steatosis and is a main risk factor in fatty liver transplantation. Adenosine receptors (ARs) are emerging as therapeutic targets in liver diseases. By using cellular and in vivo systems of hepatic steatosis and IRI, here we evaluated the effects of pharmacological A2AR and A1R activation. The A2AR agonist CGS21680 protected the primary steatotic murine hepatocyte from IR damage and the activation of ASK1 and JNK. Such an effect was attributed to a phosphatidylinositol-3-kinase (PI3K)/Akt-dependent inhibition of ASK1. By contrast, the A1R agonist CCPA enhanced IR damage, intracellular steatosis and oxidative species (OS) production, thereby further increasing the lipid/OS-dependent ASK1-JNK stimulation. The CGS2680 and CCPA effects were nullified by a genetic ASK1 downregulation in steatotic hepatoma C1C7 cells. In steatotic mice livers, CGS21680 protected against hepatic IRI and ASK1/JNK activation whereas CCPA aggravated hepatic steatosis and IRI, and enhanced ASK1 and JNK stimulation. These results evidence a novel mechanism of CGS21680-mediated hepatoprotection, i.e., the PI3K/AKT-dependent inhibition of ASK1, and they show that CGS21680 and CCPA reduces and enhances the IRI of fatty liver, respectively, by preventing or increasing the activation of the cytotoxic ASK1/JNK axis. They also indicate the selective employment of A2AR agonists as an effective therapeutic strategy to prevent IRI in human fatty liver surgery.

scholarly journals New Insights in Mechanisms and Therapeutics for Short- and Long-Term Impacts of Hepatic Ischemia Reperfusion Injury Post Liver Transplantation

2021 ◽  
Vol 22 (15) ◽  
pp. 8210
Author(s):  
Hui Liu ◽  
Kwan Man
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Graft Function ◽  
Cancer Recurrence ◽  
Short Term ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

Liver transplantation has been identified as the most effective treatment for patients with end-stage liver diseases. However, hepatic ischemia reperfusion injury (IRI) is associated with poor graft function and poses a risk of adverse clinical outcomes post transplantation. Cell death, including apoptosis, necrosis, ferroptosis and pyroptosis, is induced during the acute phase of liver IRI. The release of danger-associated molecular patterns (DAPMs) and mitochondrial dysfunction resulting from the disturbance of metabolic homeostasis initiates graft inflammation. The inflammation in the short term exacerbates hepatic damage, leading to graft dysfunction and a higher incidence of acute rejection. The subsequent changes in the graft immune environment due to hepatic IRI may result in chronic rejection, cancer recurrence and fibrogenesis in the long term. In this review, we mainly focus on new mechanisms of inflammation initiated by immune activation related to metabolic alteration in the short term during liver IRI. The latest mechanisms of cancer recurrence and fibrogenesis due to the long-term impact of inflammation in hepatic IRI is also discussed. Furthermore, the development of therapeutic strategies, including ischemia preconditioning, pharmacological inhibitors and machine perfusion, for both attenuating acute inflammatory injury and preventing late-phase disease recurrence, will be summarized in the context of clinical, translational and basic research.

scholarly journals The impact of diet-induced hepatic steatosis in a murine model of hepatic ischemia/reperfusion injury

2018 ◽  
Vol 24 (7) ◽  
pp. 908-921 ◽  
Author(s):  
Kim H. H. Liss ◽  
Kyle S. McCommis ◽  
Kari T. Chambers ◽  
Terri A. Pietka ◽  
George G. Schweitzer ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Hepatic Steatosis ◽  
Murine Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
The Impact
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