scholarly journals Differential Effects of Three Techniques for Hepatic Vascular Exclusion during Resection for Liver Cirrhosis on Hepatic Ischemia-Reperfusion Injury in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Changjun Jia ◽  
Chaoliu Dai ◽  
Hailiang Wang ◽  
Yi Wan ◽  
Yunyu Qiao ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Vascular Occlusion ◽  
Pringle Maneuver ◽  
Hepatic Ischemia ◽  
Necrosis Factor Alpha ◽  
Differential Effects ◽  
Vascular Exclusion ◽  
Hepatic Ischemia Reperfusion ◽  
Underlying Mechanisms

Background/Aims. Hepatic ischemia-reperfusion (I/R) injury is a serious concern during hepatic vascular occlusion. The objectives of this study were to assess effects of three techniques for hepatic vascular occlusion on I/R injury and to explore the underlying mechanisms. Methods. Liver cirrhotic rats had undertaken Pringle maneuver (PR), hemihepatic vascular occlusion (HH), or hepatic blood inflow occlusion without hemihepatic artery control (WH). Levels of tumor necrosis factor alpha (TNF-α), nuclear factor kappa B (NF-κB), toll-like receptor 4 (TLR4), TIR-domain-containing adapter-inducing interferon-β (TRIF), and hemeoxygenase 1 (HMOX1) were assayed. Results. The histopathologic analysis displayed that liver harm was more prominent in the PR group, but similar in the HH and WH groups. The HH and WH groups responded to hepatic I/R inflammation similarly but better than the PR group. Mechanical studies suggested that TNF-α/NF-κB signaling and TLR4/TRIF transduction pathways were associated with the differential effects. In addition, the HH and WH groups had significantly higher levels of hepatic HMOX1 (P<0.05) than the PR group. Conclusions. HH and WH confer better preservation of liver function and protection than the Pringle maneuver in combating I/R injury. Upregulation of HMOX1 may lead to better protection and clinical outcomes after liver resection.

Intrathecal morphine pretreatment ameliorated hepatic ischemia-reperfusion injury by reducing inflammation through peripheral and spinal opioid activation in rats

2020 ◽  
Author(s):  
Yuan Wang ◽  
Jueying Liu ◽  
Yifeng Qu ◽  
Yinghui Fan ◽  
Weifeng Yu
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Intrathecal Morphine ◽  
Ischemia Reperfusion ◽  
Akt Pathway ◽  
Hepatic Ischemia ◽  
Necrosis Factor Alpha ◽  
Hepatic Ischemia Reperfusion ◽  
Spinal Opioid

Abstract Background Hepatic ischemia-reperfusion injury (IRI) is a common phenomenon after liver transplantation and liver tumor surgery. Morphine provides analgesia and prevents hepatic IRI. Besides morphine in the spinal cord has the protective effect on hepatic IRI. But the mechanism has not been well characterized. This study investigated whether morphine administrated intrathecally mimic the protective effect by reducing inflammation, and whether this kind of effect was mediated by phosphatidylinositol-3-kinase (PI3K)/Akt pathway. Methods We established models of hepatic IRI and intrathel catheter insertion on Sprague-Dawley. Morphine was administrated 10min prior hepatic ischemia flowed with 6h reperfusion. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), histological changes and liver cell apoptosis assessed liver IRI. Similar maneuvers were repeated using the optimal dose and opioid receptor antagonist naloxone methiodide (NM). Serum ALT and AST, histological staining, hepatic apoptosis and serum levels of tumor necrosis factor alpha (TNF-α) and interleukin 1β (IL-1β) were assessed. Expression of Akt and its downstream protein Erk were evaluated by Western blotting. Results Morphine pretreatment intrathecally at dose of 10μg·mg -1 reduced ALT and AST levels, hepatic apoptosis, inflammation and preserved liver structure. These changes were partially reserved by NM 10min prior morphine injection. Morphine elevated the expression of Akt and Erk, however, NM did not decrease Akt and Erk expression. Conclusion Intrathecal morphine pretreatment reduced rats’ livers’ inflammation through both peripheral and spinal opioid receptors activation. The potential mechanism contributed to moderate PI3K/Akt pathway.

scholarly journals Global proteome profiling of human livers upon ischemia/reperfusion treatment

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Haijian Cai ◽  
Shunli Qi ◽  
Qi Yan ◽  
Jun Ling ◽  
Jian Du ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Metabolic Pathways ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Research Direction ◽  
Bioinformatic Analysis ◽  
Pringle Maneuver ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

AbstractHepatic ischemia/reperfusion (I/R) injury represents a major risk factor for liver transplantation and is related to graft dysfunction and acute/chronic rejection. However, a significant part of these processes remain poorly characterized. To reveal differences in the proteome during liver I/R injury, we collected human liver biopsy samples during hepatectomy before and after the Pringle maneuver and conducted a TMT-based proteomic analysis through quantitative high-throughput mass spectrometry. We used a fold-change threshold of 1.3 and a t-test p-value < 0.05 as the criteria to identify 5,257 total quantifiable proteins. The levels of 142 proteins were increased, while the levels of 103 proteins were decreased in response to hepatic I/R treatment. Bioinformatic analysis further revealed that these differentially expressed proteins are mainly involved in multiple biological functions and enzyme-regulated metabolic pathways. Most proteins whose expression was changed are related to the defense, immune and inflammatory responses as well as lipid and steroid metabolic processes. Based on this finding, we developed a panel for targeted proteomic analysis and used the parallel reaction monitoring (PRM) method, qPCR and western blotting experiments to validate alterations in the expression of some of the identified proteins. The upregulated proteins were found to be involved in immunity and inflammatory responses, and downregulated proteins were enriched in metabolic pathways. This study therefore may provide a research direction for the design of new therapeutic strategies for hepatic ischemia/reperfusion injury.

scholarly journals Alleviation of Hepatic Ischemia Reperfusion Injury by Oleanolic Acid Pretreating via Reducing HMGB1 Release and Inhibiting Apoptosis and Autophagy

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Wenwen Wang ◽  
Liwei Wu ◽  
Jingjing Li ◽  
Jie Ji ◽  
Kan Chen ◽  
...  
Keyword(s):  
Oleanolic Acid ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
High Mobility ◽  
Protective Effects ◽  
Caspase 9 ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
Underlying Mechanisms ◽  
Necrosis Factor

Hepatic ischemia reperfusion (IR) injury (IRI) occurs during liver transplantation, hepatectomy, and hemorrhagic shock. Oleanolic acid (OA) is a natural compound with antioxidant and anti-inflammatory activity that has been used to treat liver disorders in clinical practice for several years. Here, we investigated the effects and underlying mechanisms of OA in hepatic IRI. A 60-minute partial (70%) hepatic, warm, ischemic reperfusion model was established in BALB/c mice, and two doses (30 and 60 mg/kg) of OA were administered intragastrically for 7 consecutive days prior to hepatic IR. Orbital blood and liver specimens were collected at 2, 8, and 24 h after IR. The results showed that OA preconditioning significantly alleviated hepatic injury, as evidenced by decreased alanine aminotransferase and aspartate aminotransferase levels; improved histology, inhibition of JNK phosphorylation, and high mobility group box 1 (HMGB1); and tumor necrosis factor-α downregulation in hepatic IR mice. OA upregulated Bcl-2 and downregulated caspase-3, caspase-9, Bax, Beclin 1, and LC3, which play crucial roles in the regulation of apoptosis and autophagy. These findings highlighted the protective effects of OA against hepatic IRI mediated by the inhibition of apoptosis and autophagy and the release of HMGB1, which acted as a late inflammatory mediator in hepatic IRI.

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