Ischemia-reperfusion In Rat Liver Research Articles

High Intensity Aerobicexercise Preconditioning Decreases Oxidative Stress Damage Associated With Rat Liver Ischemia-reperfusion Injury

High Intensity Aerobicexercise Preconditioning Decreases Oxidative Stress Damage Associated With Rat Liver Ischemia-reperfusion Injury

Activation of the AMPK-mTOR Pathway by Astaxanthin against Cold Ischemia-Reperfusion in Rat Liver.

Activation of the AMPK-mTOR Pathway by Astaxanthin against Cold Ischemia-Reperfusion in Rat Liver.

JNK and p38 gene and protein expression during liver ischemia-reperfusion in a rat model treated with silibinin.

Signal transduction of mitogen-activated protein kinases (MAPKs) is activated during ischemia. In this study, c-Jun N-terminal Kinase (JNK) and p38 MAPK (p38) gene and protein expression were evaluated as two members of the MAPK family during liver ischemia-reperfusion in rats. Thirty-two male Wistar rats were divided into four groups of eight: Vehicle, ischemia-reperfusion (IR), ischemia-reperfusion+silibinin (IR+SILI), and SILI. The IR and IR+SILI groups differed from the other two groups in that they underwent one hour of ischemia followed by three hr of reperfusion. The Vehicle and IR groups received normal saline while the SILI and IR+SILI groups were treated with silibinin (50 mg/kg). At the end of the reperfusion time, blood and ischemic liver tissue were collected for further experiments. The expression of JNK and p38 gene, the amount of serum hepatic injury indices, and malondialdehyde (MDA) in the IR group increased significantly compared with the vehicle group. The JNK and p38 gene expression decreased significantly in the IR + SILI group compared with the IR group. Glutathione peroxidase (GPx) and total antioxidant capacity (TAC) levels decreased in the IR group while increasing in the IR+SILI group. Histological examination showed that silibinin significantly reduced the severity of hepatocyte degradation. Western blot results were completely consistent with real-time PCR results. The possible pathways of the protective effect of silibinin against hepatic ischemia damages is to reduce the expression of the p38 and JNK gene and protein.

Real-time analysis of metabolites in vivo by online extraction electrospray ionization mass spectrometry coupled to microdialysis

In vivo and real-time analysis could reflect a more real biological state, which was of great significance to the study of complex life processes. In this work, we constructed an online extraction electrospray ionization (OE-ESI) ion source as the interface of microdialysis and mass spectrometry, which realized real-time analysis of metabolites in vivo without sample pretreatment process. The ion source was consisted of three coaxial capillaries, and the parameters of the ion source were optimized. The OE-ESI ion source could simultaneously extract, desalt and ionize the analyte, successfully perform MS analysis of analyte in high salt system, and overcome the ion suppression caused by salt ion. Compared with commercial ESI MS, the OE-ESI ion source had excellent salt tolerance and stability. MD-OE-ESI MS realized the real-time MS detection of metabolites in the living body, avoiding the complex desalting process. In the rat liver ischemia-reperfusion model, a total of 24 metabolites, including glucose, glutamate, glutamine, etc., were monitored in real time mode, and their concentrations had varying degrees of change during the experimental process compared with the control group. This platform, we believed, would be helpful for real-time monitoring of biological metabolites in vivo, and had great application prospects to study physiological processes.

Effects of Propofol and Vitexin on Apoptosis in Rat Liver Ischemia Reperfusion Injury

Effects of Propofol and Vitexin on Apoptosis in Rat Liver Ischemia Reperfusion Injury

The protective effect of boric acid on cholestatic rat liver ischemia reperfusion injury.

Background/aim To evaluate the potential protective effects of boric acid (BA) in experimental cholestatic liver ischemia reperfusion (IR) injury model.Materials and methods The study included 24 female rats which were divided into 3 groups each containing 8 rats. The control group (Group 1) only received laparotomy. In the IR group (Group 2) biliary tract ligation was applied and 1 week later 45 min ischemia and 1 h reperfusion with relaparotomy without any treatment was implemented. In the treatment BA+IR group (Group 3). 1 week after the biliary ligation intraperitoneal administration of 200 mg/kg BA was given 10 min before the ischemia for 45 min and reperfusion for 1 h with relaparotomy. Liver tissue and blood samples were taken for histopathological and biochemical examination. Ischemia modified albumin (IMA), SCUBE1, total antioxidant status (TAS), and total oxidant status (TOS) levels were also examined.Results Compared to control, groups IR and BA+IR had higher serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), total, and direct bilirubin levels. Albumin value was high in the control group and low in the other groups. In terms of IMA levels there was no significant difference between groups (p > 0.05). When SCUBE-1 levels were examined groups IR and BA+IR were significantly higher than the group 1. TAS was highest in the group BA+IR whereas TOS was highest in the group IR and lower in the group BA+IR. In histopathological analysis, loss of intercellular border loss in hepatocytes, diffuse nuclear pycnosis and mild to moderate neutrophilic cell infiltration were observed in the IR group. Statistically significant dissociation, hemorrhage and severe neutrophilic cell infiltration were seen in hepatocytes of rats with IR (p < 0.05). Conclusion BA has promising results in the treatment of experimental IR injury of the cholestatic liver because of its antioxidant effects. It may be used in clinical practice after more extensive studies about the effects of BA on IR injury of the cholestatic liver.

The Effects of Esmolol on Erythrocyte Deformability in Rat Liver Ischemia-Reperfusion Injury

The Effects of Esmolol on Erythrocyte Deformability in Rat Liver Ischemia-Reperfusion Injury

Effects of magnesium sulphate on liver ischemia/reperfusion injury in a rat model

Aim: To investigate the protective efficacy of magnesium sulphate in a model of rat liver ischemia-reperfusion (I/R) injury. Method: 32 adult female Wistar-Albino rats (250 to 350 g) were used in this experimental study. Rats were divided into 4 groups according to liver ischemia and magnesium sulfate application methods. Group 1 (C); control, group 2 (M); magnesium sulphate, group 3 (I/R); liver I/R, group 4 (I/R+M); I/R + magnesium sulphate treated. The blood samples were centrifuged for the study of aspartate aminotransferase (AST), alanine aminotransferase, prothrombin time (PT), international normalized ratio (INR) troponin I, total antioxidant status (TAS), total oxidant status (TOS) assays. The livers of the animals were removed at the end of the study and samples were taken for histopathological examination. Results: AST and INR values were significantly decreased in I/R+M group compared to I/R group. There was no significant difference in ALT values of the groups. Although not statistically significant, the TAS values were increased in I/R + M group compared to I/R group rats. In addition, the value of TOS was found to be lower in I/R + M group rats. In the histopathological examination, the mean values of apoptosis and necrosis were lower in the IR+M group compared to the IR group. Conclusion: The main finding of the present study suggested that magnesium sulphate pretreatment moderately decreased the liver damage through its anti-inflammatory and anti-oxidant effects in a rat model of liver I/R.

Effect of dexmedetomidine pretreatment on JAK/STAT signaling pathway during myocardial injury induced by liver ischemia-reperfusion in rats

Objective To investigate the effect of dexmedetomidine pretreatment on Janus kinase/signal transducer and activator of transcription(JAK/STAT)signaling pathway during myocardial injury induced by liver ischemia-reperfusion(I/R)in rats. Methods Twenty-four healthy adult male Sprague-Dawley rats, aged 8-10 weeks, weighing 220-250 g, were divided into 3 groups(n=8 each)using a random number table method: sham operation group(group S), liver I/R group(group I/R), and dexmedetomidine pretreatment group(group D). The portal vein, superior and inferior vena cava, subhepatic inferior vena cava and hepatic artery were clamped, and the liver was perfused with 4 ℃ lactated Ringer′s solution for 60 min through the portal vein to establish the model of liver cold I/R in anesthetized rats.Dexmedetomidine 100 μg/kg was intraperitoneally injected at 30 min before ischemia in group D. Blood samples were collected at 8 h of reperfusion from the inferior vena cava for determination of serum cardiac troponin Ⅰ (cTnI) and heart-type fatty acid binding protein(H-FABP)concentrations(using the automatic biochemistry analyzer), tumor necrosis factor-alpha(TNF-α)and high-mobility group box 1 protein(HMGB1)concentrations(by enzyme-linked immunosorbent assay). The rats were then sacrificed, and hearts were harvested for examination of histopathological changes(with a light microscope)and for determination of the malondialdehyde(MDA)content(using thiobarbituric acid method)and superoxide dismutase(SOD)activity(by xanthine oxidase method), and expression of phosphorylated STAT1 and STAT3(p-STAT1, p-STAT3)and phosphorylated JAK2(p-JAK2)in myocardial tissues(by Western blot). Results Compared with group S, the serum concentrations of cTnI, H-FABP, TNF-α and HMGB1 were significantly increased, the MDA content was increased, the SOD activity was decreased, and the expression of p-JAK2, p-STAT1 and p-STAT3 was up-regulated in I/R and D groups(P<0.05). Compared with group I/R, the serum concentrations of cTnI, H-FABP, TNF-α and HMGB1 were significantly decreased, the MDA content was decreased, the SOD activity was increased, the expression of p-JAK2, p-STAT1 and p-STAT3 was down-regulated(P<0.05), and pathological changes of myocardium were significantly attenuated in group D. Conclusion The mechanism by which dexmedetomidine pretreatment mitigates myocardial injury induced by liver cold I/R may be related to inhibiting activation of JAK/STAT signaling pathway in rats. Key words: Dexmedetomidine; Reperfusion injury; Liver; Myocardium; Janus kinase; Activating transcription factor

Beneficial effects of remote organ ischemic preconditioning on micro-rheological parameters during liver ischemia-reperfusion in the rat.

Remote ischemic preconditioning (RIPC) can be protective against the damage. However, there is no consensus on the optimal amount of tissue, the number and duration of the ischemic cycles, and the timing of the preconditioning. The hemorheological background of the process is also unknown. To investigate the effects of remote organ ischemic preconditioning on micro-rheological parameters during liver ischemia-reperfusion in rats. In anesthetized rats 60-minute partial liver ischemia was induced with 120-minute reperfusion (Control, n = 7). In the preconditioned groups a tourniquet was applied on the left thigh for 3×10 minutes 1 hour (RIPC-1, n = 7) or 24 hours (RIPC-24, n = 7) prior to the liver ischemia. Blood samples were taken before the operation and during the reperfusion. Acid-base, hematological parameters, erythrocyte aggregation and deformability were tested. Lactate concentration significantly increased by the end of the reperfusion. Erythrocyte deformability was improved in the RIPC-1 group, erythrocyte aggregation increased during the reperfusion, particularly in the RIPC-24 group. RIPC alleviated several hemorheological changes caused by the liver I/R. However, the optimal timing of the RIPC cannot be defined based on these results.

Sevoflurane relieves hepatic ischemia-reperfusion injury by inhibiting the expression of Grp78.

Purpose: This article aimed to study the role of sevoflurane pre-conditioning in hepatic ischemia–reperfusion and its potential mechanism.Methods: Rat liver ischemia–reperfusion model was constructed. Serum TNF-α, IL-1β, IL-10, and IL-6 concentrations were detected by ELISA. Malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) in liver homogenate were determined. Hematoxylin–Eosin (HE) staining, Tunel, and immunohistochemistry were performed. Ischemia–reperfusion hepatocyte model was established. Cells transfection was conducted. Apoptosis was observed by flow cytometry. Quantitative real-time PCR (qRT-PCR) and Western blotting analysis were used.Results: Compared with I/R group, liver damage degree, liver cell apoptosis, and glucose regulatory protein 78 (Grp78) expression was obviously reduced in rats of SEV group. TNF-α, IL-1β, and IL-6 concentrations were also significantly increased (P<0.01). MDA and NO concentrations were dramatically lower (P<0.01) and SOD concentration was significantly higher (P<0.01). Apoptosis rate, Grp78, PERK, eIF2α, and p-c-JNK/JNK expression was also significantly decreased (P<0.01). Sevoflurane significantly reduced apoptosis and expression of PERK, eIF2α, p-c-JNK/JNK by inhibiting the expression of Grp78 (P<0.01).Conclusion: Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78.

Anti-oxidative and anti-inflammatory effects of Rosa Mosqueta oil supplementation in rat liver ischemia-reperfusion.

Ischemia-reperfusion (IR) is a deleterious condition associated with liver transplantation or resection that involves pro-oxidant and pro-inflammatory mechanisms. Considering that Rosa Mosqueta (RM) oil composition is rich in protective components such as α-linolenic acid (ALA) and tocopherols, we studied the effects of RM oil supplementation given prior to an IR protocol. Male Sprague-Dawley rats receiving RM oil (0.4 mL d-1) for 21 days were subjected to 1 h of ischemia followed by 20 h reperfusion. Parameters of liver injury (serum transaminases, histology), oxidative stress [liver contents of protein carbonyls, thiobarbituric acid reactants, Nrf2 activity and its target mRNA expression of heme oxygenase-1 (HO-1) and NADPH-quinone oxidoreductase-1 (NQO-1)] and inflammation [nuclear factor-κB (NF-κB) and its target mRNA expression of tumor necrosis factor-α (TNF-α) and interleukine-1β (IL-1β)] were studied. RM oil increased liver ALA and its derived EPA and DHA fatty acids' contents, with enhancement in those of α- and γ-tocopherols. IR induced inflammatory liver injury, with enhancement in serum transaminases, oxidative stress-related parameters with reduced Nrf2 signaling, and higher pro-inflammatory cytokines, indexes that were attenuated or abrogated by RM oil pretreatment. It is concluded that RM oil supplementation represents a novel non-invasive preconditioning strategy against liver injury induced by IR that has potential clinical applications in metabolic stress conditions.

The effect of tacrolimus on high mobility group box 1 after liver ischemia reperfusion in rats

The effect of tacrolimus on high mobility group box 1 after liver ischemia reperfusion in rats

Effect of dexmedetomidine on kidney injury induced by liver ischemia-reperfusion in rats

Objective To evaluate the effect of dexmedetomidine on kidney injury induced by liver ischemia-reperfusion (I/R) in rats. Methods Twenty-four healthy male Sprague-Dawley rats, weighing 220-250 g, aged 8-10 weeks, were randomly divided into 3 groups (n=8 each) using a random number table: sham operation group (group S); liver I/R group (group I/R); dexmedetomidine group (group D). In group I/R, liver I/R model was established by clamping the portal vein, hepatic artery, supra- and infra-hepatic vena cava for 40 min, followed by 6 h of reperfusion in anesthetized rats.In group D, dexmedetomidine 100 μg/kg was injected intraperitoneally at 30 min before skin incision.The equal volume of normal saline was given instead of dexmedetomidine in S and I/R groups.At 6 h of reperfusion, blood samples were collected from the infra-hepatic vena cava for determination of blood urea nitrogen (BUN) and creatinine (Cr) concentrations (by automatic biochemical analyzer) and tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10) concentrations in serum (by enzyme-linked immunosorbent assay). After blood sampling, the rats were sacrificed, and kidneys were harvested for examination of histopathological changes (with light microscope) and for determination of malondialdehyde (MDA) content (using thiobarbituric acid method) and superoxide dismutase (SOD) activity (by xanthine oxidase method), expression of activated caspase-3 (by immuno-histochemistry), and apoptotic cells (using TUNEL). Apoptotic rate was calculated. Results Compared with group S, the serum BUN, Cr and TNF-α concentrations were significantly increased, the concentration of serum IL-10 was decreased, the MDA content and apoptotic rate were increased, the SOD activity was decreased, and the expression of activated caspase-3 was up-regulated in I/R and D groups (P<0.05). Compared with group I/R, the serum BUN, Cr and TNF-α concentrations were significantly decreased, the concentration of serum IL-10 was increased, MDA content and apoptotic rate were increased, the SOD activity was decreased, the expression of activated caspase-3 was down-regulated (P<0.05), and the histopathological changes of renal tissues were attenuated in group D. Conclusion Dexmedetomidine can reduce kidney injury induced by liver I/R in rats, and the mechanism is probably related to inhibition of inflammatory responses, lipid peroxidation and cell apoptosis. Key words: Dexmedetomidine; Reperfusion injury; Liver; Kidney

Some mechanisms of the protective effect of ischemic preconditioning on rat liver ischemia-reperfusion injury.

Ischemia-reperfusion (I/R) injury is a multifactorial process that affects graft function after liver transplantation. An understanding of the mechanisms involved in I/R injury is essential for the design of therapeutic strategies to improve the outcome of liver transplantation. The generation of reactive oxygen species subsequent to reoxygenation inflicts tissue damage and initiates a cascade of deleterious cellular responses, leading to inflammation, cell death, and ultimate organ failure. Increasing experimental evidence has suggested that Kupffer cells and T-cells mediate activation of neutrophil inflammatory responses. Activated neutrophils infiltrate the injured liver in parallel with increased expression of adhesion molecules on endothelial cells. The heme oxygenase system is among the most critical of the cytoprotective mechanisms activated during cellular stress, exerting antioxidant and anti-inflammatory functions, modulating the cell cycle, and maintaining the microcirculation. Finally, the activation of toll-like receptors on Kupffer cells may play a fundamental role in exploring new therapeutic strategies based on the concept that hepatic I/R injury represents a case for host “innate” immunity. In the present study, there was a significant decrease in hepatic activity of glycogen in the I/R group as compared with corresponding values in the control group. On the other hand, there was a significant increase in the hepatic activity of glycogen in the I/R-IP (ischemic preconditioning) group as compared with corresponding values in the I/R group.

Sildenafil Attenuates Hepatocellular Injury after Liver Ischemia Reperfusion in Rats: A Preliminary Study

We evaluated the role of sildenafil in a rat liver ischemia-reperfusion model. Forty male rats were randomly allocated in four groups. The sham group underwent midline laparotomy only. In the sildenafil group, sildenafil was administered intraperitoneally 60 minutes before sham laparotomy. In the ischemia-reperfusion (I/R) group, rats were subjected to 45 minutes of hepatic ischemia followed by 120 minutes of reperfusion, while in the sild+I/R group rats were subjected to a similar pattern of I/R after the administration of sildenafil, 60 minutes before ischemia. Two hours after reperfusion, serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured and histopathological examination of the lobes subjected to ischemia as well as TUNEL staining for apoptotic bodies was performed. Additionally, myeloperoxidase (MPO) activity and the expression of intercellular adhesion molecule-1 (ICAM-1) were analyzed. Serum markers of hepatocellular injury were significantly lower in the sild+I/R group, which also exhibited lower severity of histopathological lesions and fewer apoptotic bodies, as compared to the I/R group. The I/R group showed significantly higher MPO activity and higher expression of ICAM-1, as compared to the sild+I/R group. Use of sildenafil as a preconditioning agent in a rat model of liver I/R exerted a protective effect.

The effect of ischemic precondition to IL-6 on rat liver ischemia-reperfusion injury in transplantation

ObjectiveTo investigate the effect of ischemic precondition to protect ischemia-reperfusion injury and reduce IL-6 expression in the rats liver transplantation. MethodsThe rat portal vein infusion of autologous liver transplantation model were used. The rats were divided into ischemic preconditioning rats liver transplantation group (A group), the rats liver transplantation group (B group) and the normal rat control group (C group). Then we analyzed the changes of liver function, liver microstructure and the expression of IL-6, SOD and MDA within 48 h. ResultsThe pathology of liver in group A showed lobular architecture essentially normal, the liver cells was slightly swell and no significant changes in postoperative 12 h. In transmission electron microscope (46 000×), the mitochondria of liver cells in group A became swelling, elliptical can cristae partially broken. But there still has a small amount of arrangement. While that in group, the mitochondria were swollen, became round, serious visible crest reduce or ruptured. The result of over function test showed that the serum ALT and AST levels in group A and B were both higher than that in group C at each time period, but the serum ALT and AST levels in group A were lower than that in group B. The expression changes of IL-6 in group B were higher than that in group A and B (P<0.05). The expression of MDA in group A is more obvious than that in group B (P<0.05) ConclusionsIschemic precondition could alleviate part of ischemia-reperfusion injury in the rat liver transplantation, and also could reduce IL-6 expression to protect the liver cells against liver damage and inflammatory cytokine production.

Tissue-Protective Effect of Glutamine on Hepatic Ischemia-Reperfusion Injury via Induction of Heme Oxygenase-1

Background/Aims: Glutamine showed cytoprotective activity in vitro on anoxia-reoxygenation injury via induction of heme oxygenase-1 (HO-1). We thus investigated its in vivo tissue-protective effect in a rat liver ischemia-reperfusion (I/R) model. Methods: Before the I/R procedure, animals were treated with glutamine. Liver injury was evaluated by serum liver enzymes, histological examination and apoptosis detection by transferase-mediated uridine nick end labeling staining. Meanwhile, expression and activities of HO-1 were measured by Western blot and a biochemical method. Liver blood flow was measured by using a laser Doppler flowmeter, and oxidative injury was investigated by the thiobarbituric acid-reactive substance (TBARS) assay. The inflammatory cytokine monocyte chemotactic protein (MCP)-1 was quantified by ELISA. Results: I/R caused a large increase in levels of liver enzymes, remarkably inducing the necrosis and apoptosis of liver tissue, which was markedly inhibited by glutamine, during which HO-1 was upregulated significantly, and the HO-1 inhibitor zinc protoporphyrin nullified the effect of glutamine. Liver blood flow was greatly reduced after I/R; however, it was significantly improved by glutamine. Lipid peroxidation (TBARS) in liver tissue was largely induced which was significantly lowered by glutamine. Similar results were also observed for the production of MCP-1. Conclusion: Glutamine protected tissue against oxidative injury during rat hepatic I/R, by induction of HO-1 to fulfill antioxidative and antiapoptotic effects.

Delayed Ischemic Preconditioning Protects Against Liver Ischemia–Reperfusion Injury In Vivo

Objectives Ischemic preconditioning (IP) affords resistance to liver ischemia–reperfusion (IR) injury, providing an early phase of protection. Development of delayed IP against IR injury was assessed using partial IR in rat liver. Methods The IP manuver (10 minutes of ischemia and up to 72 hours of reperfusion) was induced before 1 hour of ischemia and 20 hours of reperfusion. At the end of the reperfusion period, blood and liver samples were analyzed for serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), haptoglobin and tumor necrosis factor-α (TNF-α) levels, hepatic histology, protein carbonyl and glutathione (GSH) contents as well as nuclear factor-κB (NF-κB), and activating protein-1 (AP-1) DNA binding. Results The IP manuver significantly increased protein carbonyl/GSH ratios (275%), serum ALT (42%), and AST (58%); these changes normalized after 12 hours. Serum AST, ALT, and LDH levels were significantly increased by IR (4-, 5.6-, and 7.0-fold, respectively), with significant changes in liver histology, protein carbonyl/GSH ratio (481% enhancement), and serum TNF-α (6.1-fold increase). Delayed IP in IR animals reduced serum AST (66%), ALT (57%), and LDH (90%) and liver GSH depletion (89%), with normalization of protein carbonyl content, serum TNF-α levels, and liver histology. Enhanced AP-1/NF-κB DNA binding ratios and diminished haptoglobin expression induced by IR were normalized by IP. Conclusion These data support that delayed IP suppresses IR-induced liver injury, oxidative stress, and TNF-α response, which coincide with recovery of IR-altered signaling functions represented by normal AP-1/NF-κB DNA binding ratios and acute phase responses.

S-Nitroso-N-Acetylcysteine Ameliorates Ischemia-Reperfusion Injury In The Steatotic Liver

BACKGROUND:Steatosis is currently the most common chronic liver disease and it can aggravate ischemia-reperfusion (IR) lesions. We hypothesized that S-nitroso-N-acetylcysteine (SNAC), an NO donor component, can ameliorate cell damage from IR injury. In this paper, we report the effect of SNAC on liver IR in rats with normal livers compared to those with steatotic livers.METHODS:Thirty-four rats were divided into five groups: I (n=8), IR in normal liver; II (n=8), IR in normal liver with SNAC; III (n=9), IR in steatotic liver; IV (n=9), IR in steatotic liver with SNAC; and V (n=10), SHAN. Liver steatosis was achieved by administration of a protein-free diet. A SNAC solution was infused intraperitoneally for one hour, beginning 30 min. after partial (70%) liver ischemia. The volume of solution infused was 1 ml/100 g body weight. The animals were sacrificed four hours after reperfusion, and the liver and lung were removed for analysis. We assessed hepatic histology, mitochondrial respiration, oxidative stress (MDA), and pulmonary myeloperoxidase.RESULTS:All groups showed significant alterations compared with the group that received SHAN. The results from the steatotic SNAC group revealed a significant improvement in liver mitochondrial respiration and oxidative stress compared to the steatotic group without SNAC. No difference in myeloperoxidase was observed. Histological analysis revealed no difference between the non-steatotic groups. However, the SNAC groups showed less intraparenchymal hemorrhage than groups without SNAC (p=0.02).CONCLUSION:This study suggests that SNAC effectively protects against IR injury in the steatotic liver but not in the normal liver.