Effect of liver ischemic preconditioning in cirrhotic rats submitted to hepatic ischemia/reperfusion injury

PURPOSE: The main aim of this study was to determine the influence of ischemic preconditioning (IPC) on rat liver cirrhosis. METHODS: Cirrhosis was induced in Wistar rats by occlusion of the hepatic duct. The animals were divided into four groups of six animals each: non-cirrhotic group (simulated operation only), cirrhotic control group (simulated operation in cirrhotic rats), I/R group (40-minute ischemia without IPC), and IPC group (cirrhotic rats with ischemia, previously submitted to IPC). The IPC procedure consisted of partial hepatic ischemia for five minutes, followed by 10 minutes of reperfusion. In the case of the IPC group, the animals were submitted to liver ischemia for 40 minutes after the preconditioning procedure, followed by 2 hours of reperfusion. Blood samples were collected for measurement of serum aminotransferases (ALT and AST). The respiratory control ratio (RCR), the mitochondrial membrane potential (MMP), and malondialdehyde (MDA) values in the hepatic tissue were analyzed. Nonparametric statistical analysis was used and a value of p<0.05 was considered statistically significant. RESULTS: Ischemia did not induce significant increase in ALT and AST levels. MDA values were significantly higher in cirrhotic animals. MMP did not significantly change in cirrhosis and liver ischemia. Mitochondrial RCR decreased in liver cirrhosis, accentuated upon liver ischemia, and did not significantly change with IPC. CONCLUSION: Ischemic preconditioning does not protect the liver from hepatic injury induced by the ischemia/ reperfusion process.

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Alteration of connexins gene expression by silibinin during hepatic warm ischemia-reperfusion injury in the rat model

10.32592/ircmj.2021.23.4.250 ◽

2021 ◽

Keyword(s):

Gene Expression ◽

Reperfusion Injury ◽

Mrna Expression ◽

Normal Saline ◽

Connexin 43 ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Hepatic Tissue ◽

Control Group ◽

Hepatic Ischemia

Background: Ischemia-reperfusion injury (IRI) is an injurious phenomenon that is the primary determinant of liver dysfunction after surgery and transplantation. The present evidence demonstrated that connexin 43 (Cx43), Cx32, and Cx26 are the essential gap junction proteins involved in the liver IRI. This study aimed to characterize the beneficial effects of silibinin on Cx43, Cx32, and Cx26 gene expression during warm hepatic ischemia-reperfusion (IR). Materials and Methods: A total of 32 male Wistar rats weighing 250-300 g were randomly divided into four equal groups of eight animals in each group as follows: 1) control group (laparotomy+normal saline), 2) laparotomy+silibinin (30 mg/kg) (SILI), 3) liver IR procedure+normal saline (IR), and 4) liver IR procedure+silibinin (30 mg/kg) (IR+SILI). After 1 h of ischemia followed by 3 h of reperfusion, blood samples and tissue sections were gathered to assess the serum liver markers and evaluate the liver histological changes as well as gene expression, respectively. Results: The obtained data proved no considerable differences between control and SILI groups in all experiments. Furthermore, the gene expression of Cx26, Cx32, and Cx43 was significantly induced in the IR group, compared to the control group. Silibinin markedly reduced Cx26 and Cx32 mRNA expression, whereas increased Cx43 mRNA expression. Moreover, serum alanine aminotransferase and aspartate aminotransferase levels were markedly elevated in the IR group (P<0.001), compared to the control group. However, in the IR+SILI group, silibinin could significantly decline these elevations, compared to the IR group. In addition, silibinin diminished hepatic tissue damages during IR. Conclusion: Silibinin could attenuate liver injury through better cell-to-cell communication via lowering Cx32 and Cx26, as well as increasing Cx43 gene expression, respectively.

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Role of Remote Ischemic Preconditioning in Hepatic Ischemic Reperfusion Injury

Dose-Response ◽

10.1177/1559325820946923 ◽

2020 ◽

Vol 18 (3) ◽

pp. 155932582094692

Author(s):

Eun Kyung Choi ◽

Hoon Jung ◽

Sungmin Jeon ◽

Jung A. Lim ◽

Jungwon Lee ◽

...

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Reperfusion Injury ◽

Inflammatory Cytokines ◽

Ischemic Preconditioning ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Remote Ischemic Preconditioning ◽

Hepatic Tissue ◽

Hepatic Ischemia

The effect of remote ischemic preconditioning (RIPC) has been proposed that mediates the protective response in ischemia reperfusion injury (IRI) of various organs. In this study, we investigated the effect of RIPC in hepatic IRI, by assessing biomarker of oxidative stress and inflammatory cytokines. Moreover, we intended to demonstrate any such protective effect through nitric oxide (NO). Twenty-five rats were divided into the 5 groups: (1) Sham; (2) RIPC; (3) hepatic IRI; (4) RIPC + hepatic IRI; (5) C-PTIO, 2-(4-carboxyphenyl)-4,5dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3oxide, + RIPC + hepatic IRI. RIPC downregulated the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), histologic damage, and activity of Malondialdehyde (MDA). However, there was no significant reduction in the level of tumor necrosis factor-alpha (TNF-α) and nuclear factor kappa B (NF-κB). AST and ALT levels, and hepatic tissue morphology in the C-PTIO group showed a significant improvement compared to those of the RIPC + hepatic IRI group. The application of RIPC before hepatic ischemia downregulated the oxidative stress, not the inflammatory cytokines. Moreover, these protective effect of RIPC would be mediated through the activation of NO as well as anti-oxidant effect.

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Rosiglitazone-enriched diet did not protect liver ischemia-reperfusion injury in a rat model

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502008000400013 ◽

2008 ◽

Vol 23 (4) ◽

pp. 378-383 ◽

Cited By ~ 2

Author(s):

Antonio Roberto Franchi Teixeira ◽

Nilza Trindade Molan ◽

Marta Bellodi-Privato ◽

Ana Maria Coelho ◽

Kátia Ramos Leite ◽

...

Keyword(s):

Reperfusion Injury ◽

Rat Model ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Classical Model ◽

Control Group ◽

Standard Diet ◽

Liver Ischemia ◽

Hepatic Ischemia ◽

Histological Assessment

PURPOSE: To determine whether rosiglitazone-enriched diet offer protection in a classical model of liver ischemia-reperfusion injury in rats. METHODS: Two days before the experiment, rats were divided into 2 groups: Control Group (n=13) rats fed with standard diet; Rosi Group (n=13): rats fed with a powdered standard diet supplemented with rosiglitazone. The animals were submitted to liver ischemia-reperfusion by clamping the pedicle of median and left anterolateral lobes. After 1 hour of partial hepatic ischemia, the clamp was removed for reperfusion. After 2 or 24 hours (Control and Rosi Groups), blood was collected for enzymes and cytokines analysis. Ischemic and non-ischemic liver were collected for malondialdehyde analysis and histological assessment. Lungs were removed for tissue myeloperoxidase quantification. RESULTS: There were no statistical differences between groups for all analysed parameters. CONCLUSION: In this model, rosiglitazone-enriched diet did not protect liver against ischemia-reperfusion injury.

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Temporal changes in hepatic antioxidant enzyme activities after ischemia and reperfusion in a rat liver ischemia model

Human & Experimental Toxicology ◽

10.1177/0960327114531991 ◽

2014 ◽

Vol 34 (3) ◽

pp. 249-259 ◽

Cited By ~ 6

Author(s):

SA Saïdi ◽

S Abdelkafi ◽

S Jbahi ◽

J van Pelt ◽

A El-Feki

Keyword(s):

Fish Oil ◽

Rat Liver ◽

Antioxidant Status ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Thiobarbituric Acid ◽

Control Group ◽

Antioxidant Enzyme Activities ◽

Liver Ischemia ◽

Hepatic Ischemia

This study investigated the hypothesis that administration of tilapia fish oil diet would attenuate warm liver ischemia/reperfusion injury (IRI) and whether fish oil modulates prooxidant/antioxidant status. Male Wistar rats were subjected to 30 min of approximately 70% hepatic ischemia followed by 1, 12, and 24 h reperfusion. Rats were randomly divided into three groups: sham-operated group (SO), control–warm hepatic ischemia (WI) group, and Oil–WI group given tilapia oil for 3 weeks followed by liver IRI. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured in the plasma. Levels of thiobarbituric acid reactive substances (TBARS) and antioxidant enzymes as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities were measured in liver fractions. In the sham group, there was no enzymatic or histological change. I/R caused significant increase in serum AST, ALT, and tissue TBARS levels. As compared to the control group, animals treated with tilapia oil experienced a significant decrease ( p < 0.05) in AST and ALT levels in reperfusion periods. Tissue TBARS levels in Oil–WI group were significantly ( p < 0.05) reduced as compared to control group at 60 min after reperfusion. After ischemia, 1, 12, and 24 h of reperfusion, CAT, SOD, and GPx values were the lowest in the Oil–WI group and highest in the control group and were statistically significant ( p < 0.05). Histological analysis also revealed that fish oil provided some protection compared with the control group. Tilapia oil exerts a protective effect during the early phase of reperfusion, and it modulates prooxidant/antioxidant status of rat liver subjected to warm IRI.

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Effect of remote ischemic preconditioning on hepatic ischemia-reperfusion injury in patients undergoing liver resection: a randomized controlled trial

Minerva Anestesiologica ◽

10.23736/s0375-9393.19.13838-2 ◽

2020 ◽

Vol 86 (3) ◽

Cited By ~ 1

Author(s):

Guilin Wu ◽

Mo Chen ◽

Xiaoqiang Wang ◽

Erliang Kong ◽

Weifeng Yu ◽

...

Keyword(s):

Randomized Controlled Trial ◽

Liver Resection ◽

Reperfusion Injury ◽

Ischemic Preconditioning ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Controlled Trial ◽

Hepatic Ischemia ◽

Randomized Controlled ◽

Hepatic Ischemia Reperfusion

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Galangin Alleviates Liver Ischemia-Reperfusion Injury in a Rat Model by Mediating the PI3K/AKT Pathway

Cellular Physiology and Biochemistry ◽

10.1159/000495553 ◽

2018 ◽

Vol 51 (3) ◽

pp. 1354-1363 ◽

Cited By ~ 7

Author(s):

Yang Li ◽

Liquan Tong ◽

Jingyan Zhang ◽

Yafeng Zhang ◽

Feng Zhang

Keyword(s):

Oxidative Stress ◽

Ischemia Reperfusion Injury ◽

Hepatic Duct ◽

Ischemia Reperfusion ◽

Trauma Surgery ◽

Liver Ischemia ◽

Western Blots ◽

Phosphorylated Akt ◽

Related Proteins

Background/Aims: Liver ischemia-reperfusion (I/R) injury is a pathological process that often occurs during liver and trauma surgery. There are numerous causes of liver I/R injury, but the mechanism is unknown. Galangin (GA) is a flavonoid, a polyphenolic compound widely distributed in medicinal herbs that has anti-inflammatory, antioxidant, and antitumor activity. This study evaluated the protective effect of GA on hepatic I/R injury. Methods: An I/R model was created in male Wistar rats by clamping the hepatoportal vein, hepatic artery and hepatic duct for 30 min followed by reperfusion for 2 h. A hypoxia/restoration (H/R) model was established in buffalo rat liver (BRL) cells by hypoxia for 4 h followed by normoxic conditions for 10 h. The extent of liver injury was assayed by serum ALT/AST, hepatic histology, and MPO activity. Oxidative stress was assayed by serum superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA). Expression of apoptosis-related proteins in BRL cells was assayed in western blots. Expression of AKT and p-AKT proteins in vivo and vitro were assayed in western blots. Results: GA significantly decreased ALT/AST expression, reversed changes in oxidative stress markers induced by I/R, and mediated caspase-3 activity expression of apoptosis-related proteins in vivo and in vitro. Methylthiazol tetrazolium (MTT) assay, flow cytometry, and Hoechst 33258 staining confirmed that GA inhibited apoptosis of BRL cells. GA also increased the expression of phosphorylated AKT after H/R. Conclusion: GA reduced liver I/R injury both in vivo and vitro and inhibited BRL cell apoptosis. PI3K/AKT signaling have been involved. GA may protect against liver I/R and be a potential therapeutic candidate.

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