scholarly journals Sevoflurane alleviates liver ischemia reperfusion injury through inactivation of the TRAF6/NF-κB signaling pathway

2021 ◽  
Vol 20 (10) ◽  
pp. 2043-2048
Author(s):  
Hongqiang Liu ◽  
Ying Yuan ◽  
Dan Rao
Keyword(s):  
Protein Expression ◽  
Reperfusion Injury ◽  
Liver Tissue ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Inflammatory Cells ◽  
Liver Ischemia ◽  
Pathological Changes ◽  
Tnf Α

Purpose: To evaluate the role and mechanism of action of sevoflurane in liver ischemia reperfusion injury.Methods: Rats were pretreated with sevoflurane and then underwent liver ischemia followed by reperfusion to establish an animal model of liver ischemia reperfusion injury. Pathological changes in liver tissues were investigated by hematoxylin and eosin (H & E) staining, and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined using a chemistryanalyzer. ELISA was used to determine the levels of myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), IL-6, superoxide (SOD), malonaldehyde (MDA), catalase (CAT), and glutathione (GSH).Results: Pathological changes in liver tissue, including sinusoidal congestion, vacuole formation, and infiltration of inflammatory cells and lymphocytes, were identified in rats post-ischemia reperfusion injury. In addition, serum ALT and AST levels increased following ischemia reperfusion injury. However, administration of sevoflurane ameliorated the pathological liver damage and decreased the serum ALTand AST levels induced by ischemia reperfusion. Pro- inflammatory cytokines, such as MPO, TNF-α, IL- 1β, and IL-6 were upregulated in rats following ischemia reperfusion injury, and this upregulation was reversed by sevoflurane administration. Sevoflurane administration also attenuated the ischemia reperfusion-induced increase in MDA and decrease in SOD, CAT, and GSH. Ischemia reperfusionrepressed IκBα protein expression and promoted protein expression of TNF receptor associated factor 6 (TRAF6), phospho (p)-IκBα, and p-p65 in liver tissue. However, sevoflurane reversed the effect of ischemia reperfusion on IκBα, TRAF6, p-IκBα, and p-65 expression.Conclusion: Sevoflurane administration reduced pathological liver injury post-ischemia reperfusion bysuppressing the inflammatory response and oxidative stress through inactivation of the TRAF6/NF-κB pathway.

scholarly journals Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

2020 ◽  
Author(s):  
Xiujing Zhang ◽  
Wei Wang ◽  
Jie Tang ◽  
Qin Xie ◽  
Di Ma
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pathological Changes ◽  
Apoptosis Protein ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Trillium Tschonoskii

Abstract BackgroundTo investigate the effect and possible mechanisms of total saponins from Trillium Tschonoskii Maxim. (TST) on myocardial ischemia reperfusion injury in rat.Methods and ResultsRats were pre-treated with TST in 100 and 200 mg/kg, respectively. After 14 days intragastric administration, the model of myocardial ischemia-reperfusion injury was established by ligation of the left anterior descending coronary artery for 30 min and then releasing the ligated artery for 120 min. The hemodynamic indexes, anti-oxidation index, and the anti-inflammation factors were detected. Pathological changes in myocardia tissue were observed by H&E staining. Apoptosis protein expression of caspase 3, 9, 12, AMPK, phosphorylation AMPK (p-AMPK) and Sirt1 was detected by Western blot. Pretreating the rats with TST dramatically decreased the levels of MDA, TNF-α, IL-6 and IL-1β, increased the levels of SOD and GSH-Px, and the apoptosis protein expression were all significantly decreased. In addition, the protein expression of p-AMPK and Sirt1 were markedly increased in TST pre-treated group. Furthermore, TST pre-treatment also improved the histopathological changes.ConclusionTST protect the myocardium by reducing the levels of inflammation factors, peroxides and cell apoptosis, increasing the anti-oxidase, and improving the pathological changes. The possible mechanism maybe through the activating of the AMPK/Sirt1 signaling pathway.

scholarly journals Role of cytokines in myocardial ischemia and reperfusion

1997 ◽  
Vol 6 (3) ◽  
pp. 175-183 ◽  
Author(s):  
H. S. Sharma ◽  
D. K. Das
Keyword(s):  
Myocardial Infarction ◽  
Growth Factor ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Membrane Damage ◽  
Inflammatory Cells ◽  
Myocardial Ischemia And Reperfusion ◽  
Tnf Α

Mediators of myocardial inflammation, predominantly cytokines, have for many years been implicated in the healing processes after infarction. In recent years, however, more attention has been paid to the possibility that the inflammation may result in deleterious complications for myocardial infarction. The proinflammatory cytokines may mediate myocardial dysfunction associated with myocardial infarction, severe congestive heart failure, and sepsis. A growing body of literature suggests that inflammatory mediators could play a crucial role in ischemia–reperfusion injury. Furthermore, ischemia–reperfusion not only results in the local transcriptional and translational upregulation of cytokines but also leads to tissue infiltration by inflammatory cells. These inflammatory cells are a ready source of a variety of cytokines which could be lethal for the cardiomyocytes. At the cellular level it has been shown that hypoxia causes a series of well documented changes in cardiomyocytes that includes loss of contractility, changes in lipid metabolism and subsequent irreversible cell membrane damage leading to cell death. For instance, hypoxic cardiomyocytes produce interleukin-6 (IL-6) which could contribute to the myocardial dysfunction observed in ischemia reperfusion injury. Ischemia followed by reperfusion induces a number of other multi-potent cytokines, such as IL-1, IL-8, tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1) as well as an angiogenic cytokine/ growth factor, vascular endothelial growth factor (VEGF), in the heart. Intrestingly, these multipotent cytokines (e.g. TNF-α) may induce an adaptive cytoprotective response in the reperfused myocardium. In this review, we have included a number of cytokines that may contribute to ventricular dysfunction and/or to the cytoprotective and adaptive changes in the reperfused heart.

Reduction of Liver Ischemia Reperfusion Injury by Silencing of TNF-α Gene with shRNA

2012 ◽  
Vol 176 (2) ◽  
pp. 614-620 ◽  
Author(s):  
Roberto Hernandez-Alejandro ◽  
Xusheng Zhang ◽  
Kris P. Croome ◽  
Xiufen Zheng ◽  
Jeremy Parfitt ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Ischemia ◽  
Tnf Α

Glutathione protects mitochondrion and alleviates liver ischemia-reperfusion injury in rats

2015 ◽  
Vol 36 (12) ◽  
pp. 1300
Author(s):  
Lin-lin CAI ◽  
Hai-long FU ◽  
Qing-qing ZHANG ◽  
Yong-hua LI ◽  
Qiu-feng ZHU ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Ischemia

Arrb1 Ameliorates Liver Ischemia/Reperfusion Injury Via Interacting with TRAF6 in Hepatocytes

2019 ◽  
Author(s):  
Xiaoliang Xu ◽  
Zechuan Zhang ◽  
Yijun Lu ◽  
Qikai Sun ◽  
Yang Liu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Ischemia

scholarly journals Dynamics of hyaluronan, CD44, and inflammatory cells in the rat kidney after ischemia/reperfusion injury

2006 ◽  
Author(s):  
Anne-Emilie Declèves ◽  
Nathalie Caron ◽  
Denis Nonclercq ◽  
Alexandre Legrand ◽  
Gérard Toubeau ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Inflammatory Cells

Beneficial effects of natural compounds on experimental liver ischemia-reperfusion injury

2021 ◽  
Author(s):  
Camila Dossi ◽  
Romina Vargas ◽  
Rodrigo Valenzuela ◽  
Luis Videla
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Natural Compounds ◽  
Liver Ischemia ◽  
Hepatic Surgery ◽  
Beneficial Effects ◽  
Underlying Mechanisms ◽  
Experimental Liver

Liver ischemia-reperfusion injury (IRI) is a phenomenon inherent to hepatic surgery that severely compromises the organ functionality, whose underlying mechanisms involve cellular and molecular interrelated processes leading to the development...

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