scholarly journals Electroacupuncture in the Contralesional Hemisphere Improves Neurological Function Involving GABA in Ischemia–Reperfusion Injury Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Chung-Hsiang Liu ◽  
Wen-Ling Liao ◽  
Shan-Yu Su ◽  
Wei-Liang Chen ◽  
Ching-Liang Hsieh
Keyword(s):  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neurological Status ◽  
Test Time ◽  
Gamma Aminobutyric Acid ◽  
Gaba A ◽  
Infarction Volume ◽  
The Difference

This study investigated the effect and mechanism of electroacupuncture (EA) on the contralesional hemisphere in rats with ischemic stroke. EA of 2 Hz was applied on the contralesionally Luoque (BL8) and Tongtian (BL7) acupoints of the scalp to investigate the neurological status and mechanism in ischemia–reperfusion injury rats. The differences in the neurological deficit score and Rotarod test time between days 3 and 15 after reperfusion were significantly lower in the sham group (0.00 (−1.00, 0.00) and 3.53 (−0.39, 7.48) second, respectively) than in the EA group (−4.00 (−4.00, −3.00) and 44.80 (41.69, 54.13) second, respectively, both p < 0.001 ). The ratio of infarction volume was 0.19 ± 0.04 in the sham group greater than 0.07 ± 0.04 in the EA group ( p < 0.001 ). On day 15, in the cerebral cortex of the lesioned hemisphere, the gamma-aminobutyric acid (GABA)-A/actin ratio in the normal group (1.11 ± 0.36) was higher than that in the sham group (0.38 ± 0.07, p < 0.05 ) and similar to that in the EA group (0.69 ± 0.18, p > 0.05 ); the difference between the EA and sham groups was significant ( p < 0.05 ). EA of 2 Hz on the BL8 and BL7 acupoints on the contralesional scalp can improve motor function and also can reduce infarction volume, and this effect of EA, and that GABA-A, plays at least a partial role in ischemia–reperfusion injury rats.

scholarly journals The Protective Effects of Alpha-Lipoic Acid and Coenzyme Q10Combination on Ovarian Ischemia-Reperfusion Injury: An Experimental Study

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Ahmet Ali Tuncer ◽  
Mehmet Fatih Bozkurt ◽  
Tulay Koken ◽  
Nurhan Dogan ◽  
Mine Kanat Pektaş ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Lipoic Acid ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ovarian Tissue ◽  
Coenzyme Q ◽  
Alpha Lipoic Acid ◽  
Oxide Synthase

Objective. This study aims to evaluate whether alpha-lipoic acid and/or coenzyme Q10can protect the prepubertal ovarian tissue from ischemia-reperfusion injury in an experimental rat model of ovarian torsion.Materials and Methods. Forty-two female preadolescent Wistar-Albino rats were divided into 6 equal groups randomly. The sham group had laparotomy without torsion; the other groups had torsion/detorsion procedure. After undergoing torsion, group 2 received saline, group 3 received olive oil, group 4 received alpha-lipoic acid, group 5 received coenzyme Q10, and group 6 received both alpha-lipoic acid and coenzyme Q10orally. The oxidant-antioxidant statuses of these groups were compared using biochemical measurement of oxidized/reduced glutathione, glutathione peroxidase and malondialdehyde, pathological evaluation of damage and apoptosis within the ovarian tissue, and immunohistochemical assessment of nitric oxide synthase.Results. The left ovaries of the alpha-lipoic acid + coenzyme Q10group had significantly lower apoptosis scores and significantly higher nitric oxide synthase content than the left ovaries of the control groups. The alpha-lipoic acid + coenzyme Q10group had significantly higher glutathione peroxidase levels and serum malondialdehyde concentrations than the sham group.Conclusions. The combination of alpha-lipoic acid and coenzyme Q10has beneficial effects on oxidative stress induced by ischemia-reperfusion injury related to ovarian torsion.

Effects of dextran on microvascular ischemia-reperfusion injury in striated muscle

1997 ◽  
Vol 272 (4) ◽  
pp. H1710-H1716 ◽  
Author(s):  
M. Steinbauer ◽  
A. G. Harris ◽  
K. Messmer
Keyword(s):  
Molecular Weight ◽  
Reperfusion Injury ◽  
Striated Muscle ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Capillary Density ◽  
Vessel Diameter ◽  
Functional Capillary Density ◽  
Molecular Weights ◽  
The Difference

The objectives of this study were 1) to elucidate the effects of dextran (Dx) at a nonhemodiluting dose of 5 mg/kg on ischemia-reperfusion injury in striated muscle and 2) to investigate whether the effects are dependent on the molecular weight of Dx. We used the model of a 4-h pressure-induced ischemia in the hamster skinfold chamber. By means of intravital microscopy the following parameters were assessed: vessel diameter, red blood cell velocity, rolling and adherent leukocytes, macromolecular extravasation, and functional capillary density. The animals received a continuous infusion (total dose 5 mg/kg) of dextran of different molecular weights or equivalent volumes of saline. Seven groups were studied: NaCl (control, n = 6), Dx 1 (n = 6), Dx 40 (n = 7), Dx 60 (n = 6), Dx 70 (n = 7), Dx 110 (n = 7), and Dx 150 (n = 7). Leukocyte rolling was reduced by all Dx fractions, the difference from the control reaching significance 0.5 h after reperfusion in the Dx 60, Dx 70, and Dx 110 group, whereas leukocyte adherence was attenuated by > 40,000-mol-wt Dx at 0.5 h after reperfusion. Concomitantly, functional capillary density tended to improve after treatment with > or = 40,000-mol-wt Dx. However, all Dx fractions studied failed to reduce postischemic macromolecular extravasation. These results provide evidence that Dx at 5 mg/kg attenuates postischemic microvascular disturbances; this effect is molecular weight dependent.

Effects of curcumin on acute spinal cord ischemia-reperfusion injury in rabbits

2014 ◽  
Vol 20 (4) ◽  
pp. 464-470 ◽  
Author(s):  
Gokhan Kurt ◽  
Zuhal Yildirim ◽  
Berker Cemil ◽  
Emrah Celtikci ◽  
Gulnur Take Kaplanoglu
Keyword(s):  
Spinal Cord ◽  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Histological Evaluation ◽  
Spinal Cord Tissue ◽  
Tnf Α ◽  
Nitrite Nitrate

Object The object of this study was to conduct a prospective, randomized, laboratory investigation of the neuroprotective effects of curcumin functionally, biochemically, and histologically in an experimental acute spinal cord ischemia-reperfusion injury on rabbits. Methods Eighteen rabbits were randomly assigned to 1 of 3 groups: the sham group, the ischemia-reperfusion group, or the curcumin group. Spinal cord ischemia was induced by applying an infrarenal aortic cross-clamp for 30 minutes. At 48 hours after ischemia, neurological function was evaluated with modified Tarlov criteria. Biochemical changes in the spinal cord and plasma were observed by measuring levels of malondialdehyde (MDA), advanced oxidation protein products (AOPP), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitrite/nitrate, and tumor necrosis factor-α (TNF-α). Histological changes were examined with H & E staining. Immunohistochemical staining with antibodies against caspase-3 was performed to evaluate cell apoptosis after ischemia. Results In the curcumin group, neurological outcome scores were statistically significantly better compared with the ischemia-reperfusion group. In the ischemia-reperfusion group, MDA, AOPP, and nitrite/nitrate levels were significantly elevated in the spinal cord tissue and the plasma by the induction of ischemia-reperfusion. The curcumin treatment significantly prevented the ischemia-reperfusion–induced elevation of nitrite/nitrate and TNF-α. In addition, the spinal cord tissue and the plasma SOD, GSH, and CAT levels were found to be preserved in the curcumin group and not statistically different from those of the sham group. Histological evaluation of the tissues also demonstrated a decrease in axonal damage, neuronal degeneration, and glial cell infiltration after curcumin administration. Conclusions Although further studies including different dose regimens and time intervals are required, curcumin could attenuate a spinal cord ischemia-reperfusion injury in rabbits via reducing oxidative products and proinflammatory cytokines, as well as increasing activities of antioxidant enzymes and preventing apoptotic cell death.

Abstract 2473: Ubiquitin Ligase Huwe1 Modulates Prongf/p75ntr In Monkey Cerebral Ischemia-reperfusion Injury

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Qian G He ◽  
Lihua Yu ◽  
Wenming Xu ◽  
Jiachuan Duan ◽  
Jian Guo ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ubiquitin Ligase ◽  
Cell Apoptosis ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Model Group ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Background: Ischemic neuronal cell apoptosis is a principal neuropathological feature of stroke. The p75 neurotrophin receptor (p75NTR) induces apoptosis associated with JNK-p53-BAX pathway, p53 is the substrate of the HECT domain-containing E3 ubiquitin ligase Huwe1. Recent studies suggest that the precursor form of NGF (proNGF) binds to p75NTR, and withhold the interaction of proNGF/p75NTR is efficacious in reducing neuronal apoptosis. Studies on tumor and phylogeny, show that Huwe1 highly expressed in CNS, playing a role in the regulation of cell apoptosis and a variety of injury types. Our aim is to examine whether Huwe1 modulates proNGF/p75NTR in cerebral ischemia-reperfusion injury. Methods: Eight male rhesus monkey were randomly divided into two groups: sham(n=2) and model group(n=6). The model group was administered equal volume of PBS, or silencing huwe1 Lentiviral Vector or empty Vector in right caudatum and putamen using brain stereotaxic technology and subjected to transient right middle cerebral artery occlusion (MCAO) a month later. A battery of neurological evaluation and magnetic resonance imaging (MRI) were employed to evaluate animals. Animals were sacrificed 3 days after MCAO and brains were processed for testing transfection efficiency using GFP fluorescence and evaluating cell apoptosis using TUNEL staining. The related factors in caudatum, putamen, temporal lobe and hippocampus was analyzed with QPCR, western blotting with loading control GADPH, and Immunohistochemistry. Results: The model group showed significant functional deficit than sham group with neurological evaluation (p<0.05), whereas the silencing Huwe1 group’s was the most serious. In right caudatum and putament, ischemia-reperfusion injury increased the number of TUNEL+cells(p<0.05 vs sham group) and upregulation of huwe1, proNGF and p75NTR in protein and nucleotides level (p<0.05 vs sham group), but silencing Huwe1 group increased TUNEL+cells most significantly, produced profound modulation with decreased expression of Huwe1 and obvious upregulation of proNGF and p75NTR(p<0.05 vs PBS or empty Vector group) ( Figure 1 ). However, there is no significant difference in other positions (data not show). Conclusions: Huwe1 modulates proNGF/p75NTR in the cerebral ischemia-reperfusion injury, and p53 may be as a indirect fator involved in this process. Our findings provide a novel mechanism in regulating proNGF/p75NTR signaling, suggesting its potential therapeutic target in ischemic stroke.

scholarly journals miR-155 Knockdown Protects against Cerebral Ischemia and Reperfusion Injury by Targeting MafB

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Li Zhang ◽  
Chao Liu ◽  
Chao Huang ◽  
Xiaohui Xu ◽  
Junfang Teng
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Mouse Brain ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Invasion And Migration ◽  
Infarction Volume ◽  
Cox 2 ◽  
And Migration ◽  
Brain Tissues

Background. Studies have elucidated that the variable expression levels of miRNAs influence the inflammatory process in ischemic stroke. Nevertheless, the impact and potential mechanism of miR-155 in cerebral ischemia-reperfusion injury (CIRI) keep to be incompletely known. Methods. The levels of miR-155 and MafB were determined via qRT-PCR, western blot, or immunohistochemistry assays in plasma of patients with CIRI, oxygen glucose deprivation/reoxygenation (OGD/R) induced SH-SY5Y cells, and mouse models with middle cerebral artery occlusion (MCAO). The association between miR-155 and MafB was validated via dual-luciferase reporter and western blot assays. Cell viability, apoptosis, invasion, and migration were evaluated through MTT, flow cytometry, Transwell and wound healing assays. Infarction volume was measured in MCAO mouse brain tissues by TTC assay. The expression of inflammatory mediators was measured by ELISA in cells and brain tissues. Results. miR-155 level was upregulated whereas MafB was downregulated in the plasma of patients with CIRI, OGD/R-induced SH-SY5Y cells, also as mouse models with MCAO injury. Mechanistically, miR-155 directly targeted 3’UTR of MafB and restrained MafB expression in OGD/R injury SH-SY5Y cells. Downregulation of miR-155 attenuated OGD/R-induced injury through increasing proliferation, inhibiting apoptosis, enhancing invasion and migration abilities, and constraining the expression of inflammatory mediators (IL-1β, IL-6, and TNF-α) and inflammatory enzymes (iNOS and COX-2) in SH-SY5Y cells following OGD/R, while MafB inhibition reversed the protective effects. In vivo, downregulating miR-155 reduced the infarction volume in the MACO mouse brain. Furthermore, miR-155 knockdown inhibited the IL-1β, IL-6, TNF-α, iNOS, and COX-2 in the MACO mouse brain tissues. Conclusion. Our results suggest that miR-155 knockdown alleviated ischemia-reperfusion injury by targeting MafB to improve the neurological function and inhibit inflammation response, highlighting a novel therapeutic strategist for CIRI.

scholarly journals Lung Inflation With Hydrogen During the Cold Ischemia Phase Alleviates Lung Ischemia-Reperfusion Injury by Inhibiting Pyroptosis in Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Panpan Zheng ◽  
Jiyu Kang ◽  
Entong Xing ◽  
Bin Zheng ◽  
Xueyao Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Lung Transplantation ◽  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Cold Ischemia ◽  
Lung Inflation

Background: Lung inflation with hydrogen is an effective method to protect donor lungs from lung ischemia-reperfusion injury (IRI). This study aimed to examine the effect of lung inflation with 3% hydrogen during the cold ischemia phase on pyroptosis in lung grafts of rats.Methods: Adult male Wistar rats were randomly divided into the sham group, the control group, the oxygen (O2) group, and the hydrogen (H2) group. The sham group underwent thoracotomy but no lung transplantation. In the control group, the donor lungs were deflated for 2 h. In the O2 and H2 groups, the donor lungs were inflated with 40% O2 + 60% N2 and 3% H2 + 40% O2 + 57% N2, respectively, at 10 ml/kg, and the gas was replaced every 20 min during the cold ischemia phase for 2 h. Two hours after orthotopic lung transplantation, the recipients were euthanized.Results: Compared with the control group, the O2 and H2 groups improved oxygenation indices, decreases the inflammatory response and oxidative stress, reduced lung injury, and improved pressure-volume (P-V) curves. H2 had a better protective effect than O2. Furthermore, the levels of the pyroptosis-related proteins selective nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), cysteinyl aspartate specific proteinase (caspase)-1 p20, and the N-terminal of gasdermin D (GSDMD-N) were decreased in the H2 group.Conclusion: Lung inflation with 3% hydrogen during the cold ischemia phase inhibited the inflammatory response, oxidative stress, and pyroptosis and improved the function of the graft. Inhibiting reactive oxygen species (ROS) production may be the main mechanism of the antipyroptotic effect of hydrogen.

Protective effect of Shengmai injection on myocardial endothelial cell glycoprotein detachment after myocardial ischemia-reperfusion injury in isolated rat hearts

Perfusion ◽  
2020 ◽  
pp. 026765912096592
Author(s):  
Qi Chen ◽  
Ping Zhang ◽  
Qiu-Xia Xiao ◽  
Qing Liu ◽  
Ying Zhang
Keyword(s):  
Endothelial Cell ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Stress Injury ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Objective: To investigate effects of Shengmai injection (SMI) postconditioning on myocardial ischemia-reperfusion injury (MIRI) in isolated rat hearts. Materials and methods: A total of thirty isolated hearts were randomly divided into three groups: Sham group, I/R group and SMI group. Sham group was continuously perfused with K-H solution for 120 minutes. I/R group and SMI group were given balanced perfusion for 30 min followed by reperfusion for 60 min, with an interval of 30 min, and those in the SMI group were given postconditioning with 1% SMI during the first 10 min of reperfusion. The left ventricular function, markers of myocardial injury, endothelial cell injury and oxidative stress injury were measured at 30 minutes after equilibration (t0), 30 minutes after ischemia (t2) and 60 minutes after reperfusion (t3). Results: The results showed that there was no significant difference for all observation indexes at t0. Compared with the Sham group, real portfolio project and coronary arterial flow rate and the activity of superoxide dismutase were significantly decreased in the I/R group, whereas those in the SMI group were significantly higher. Left ventricular end-diastolic pressure, the concentrate of malondialdehyde, lactate dehydrogenase, cTn-I, hyaluronic acid, heparin sulphate, syndecan-1 in the I/R group were markedly higher than those in the Sham group, whereas those in the SMI group were significantly lower. Conclusion: In summary, the present study indicated that 1% SMI postconditioning can alleviate the detachment of endothelial cell glycoprotein envelope induced by myocardial ischemia-reperfusion injury, and its mechanism is probably related to the inhibition of the oxidative stress injury.

scholarly journals Visnagin ameliorates myocardial ischemia/reperfusion injury through the promotion of autophagy and the inhibition of apoptosis

2020 ◽  
Vol 64 (s2) ◽  
Author(s):  
Hai-rong Fu ◽  
Xiao-shan Li ◽  
Yong-hui Zhang ◽  
Bin-bin Feng ◽  
Lian-hong Pan
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Protective Effect ◽  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Tunel Staining ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Visnagin is a furanochromone and one of the main compounds of Ammi visnaga L. that had been used to treat nephrolithiasis in Ancient Egypt. Nowadays, visnagin was widely used to treat angina pectoris, urolithiasis and hypertriglyceridemia. The potential mechanisms of visnagin involved in inflammation and cardiovascular disease were also identified. But the protective effect of visnagin on myocardial ischemia/reperfusion injury has not been confirmed. Our aim was, for the first time, to investigate the potential protective effect of visnagin on cardiac function after myocardial ischemia-reperfusion injury in a rat model, and to identify its underlying mechanism involving the inhibition of apoptosis and induction of autophagy. Thirty SD rats were randomly divided into sham group, ischemia/reperfusion group (IR), ischemia/reperfusion with visnagin (IR + visnagin) group. Myocardial ischemia/Reperfusion injury model was established. Hemodynamic measurements and echocardiography were used to analyze cardiac function, TUNEL staining and caspase activity, LC3 dots were detected with immunofluorescence staining, LC3 expression was evaluated by western blot analysis, transmission electron microscopy (TEM) was used to detect autophagosomes. Compared with the sham group and visnagin group, the cardiac dysfunction, LC3II, autophagy flow in the IR+ visnagin group increased significantly (P<0.01), but the activity of caspase-3 and caspase-9 and the apoptotic in the IR + visnagin group decreased significantly (P<0.01). In conclusion, visnagin may play a protective role in ischemia/reperfusion injury by inducing autophagy and reducing apoptosis.

scholarly journals Scintigraphic, histopathologic and biochemical evaluation of lycopene effects on renal ischemia reperfusion injury in rats

2017 ◽  
Vol 145 (3-4) ◽  
pp. 153-158 ◽  
Author(s):  
Murat Sadic ◽  
Hasan Atilgan ◽  
Arif Aydin ◽  
Gökhan Koca ◽  
Meliha Korkmaz ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Renal Tissue ◽  
Renal Ischemia ◽  
Control Group ◽  
Albino Rats ◽  
Renal Ischemia Reperfusion Injury

Introduction/Objective. Medical protection of kidneys against ischemia reperfusion injury is very important. Many agents have been used for the protection of ischemia reperfusion renal tissue injury. We aimed to evaluate the radioprotective effect of lycopene on kidneys in ischemia reperfusion injury with histopathological, biochemical, and scintigraphic parameters. Methods. Twenty-one Wistar male albino rats were divided into the following three groups: lycopene, control, and sham group. In the lycopene group, lycopene was started three days before right renal ischemia reperfusion injury and continued for 15 days. In the control group, right renal ischemia reperfusion injury was applied with no medication. In the sham group, neither right renal ischemia reperfusion injury nor medication were applied. On the 15th day, all rats were sacrificed after 99mTc-dimercaptosuccinic acid (DMSA) scintigraphies were taken. Histopathological, biochemical, and scintigraphic evaluations were made. Results. The histopathological score was lower in the lycopene group. In biochemical analysis, myeloperoxidase levels were lower in the lycopene group than in the control group, but not statistically significant. Malondialdehyde and nitrite levels were lower in the lycopene group than in the control group. The postoperative mean 99mTc-DMSA uptake values were 44.82 ? 1.84 in the lycopene group, 38.92 ? 1.17 in the control group, and 50.21 ? 1.35 in the sham group. DMSA uptake values were higher in the lycopene group than in the control group. Conclusion. Lycopene seems to be an effective agent for protection of kidneys in ischemia reperfusion injury as demonstrated by the histopathological, biochemical, and scintigraphic parameters.

scholarly journals Anti-Inflammatory and Antioxidant Effect of Eucommia ulmoides Polysaccharide in Hepatic Ischemia-Reperfusion Injury by Regulating ROS and the TLR-4-NF-κB Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Weidong Gao ◽  
Zanjie Feng ◽  
Shilong Zhang ◽  
Bo Wu ◽  
Xin Geng ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Eucommia Ulmoides ◽  
Hepatic Ischemia ◽  
Sd Rats ◽  
Anti Inflammatory ◽  
Hepatic Ischemia Reperfusion

Eucommia ulmoides polysaccharide (EUP) has been shown to have anti-inflammatory and antioxidant effects. However, the mechanism underlying these effects has rarely been reported, and whether EUP can reduce liver injury in hepatic ischemia-reperfusion injury (HIRI) has not been reported. In this study, 40 Sprague-Dawley (SD) rats were randomly divided into 5 groups: the sham group, ischemia-reperfusion (I/R) group, and three EUP pretreatment groups (320 mg/kg, 160 mg/kg, and 80 mg/kg). SD rats were pretreated with EUP by gavage once a day prior to I/R injury for 10 days. Except for the sham group, blood flow in the middle and left liver lobes was blocked in all the other groups, resulting in 70% liver ischemia, and the ischemia and reperfusion times were 1 h and 4 h, respectively. Ischemic liver tissue and serum were obtained to detect biochemical markers and liver histopathological damage. Compared with the I/R group, after EUP pretreatment, serum alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor-α, and interleukin-1β levels were significantly decreased, malondialdehyde levels in liver tissues were significantly decreased, superoxide dismutase levels were significantly increased, and the area of liver necrosis was notably reduced. To understand the specific mechanism involved, we determined the levels of Toll-like receptor- (TLR-) 4-nuclear factor-kappaB (NF-κB) pathway-associated proteins in vivo and in vitro. The data showed that EUP can reduce liver damage by decreasing ROS levels and inhibiting TLR-4-NF-κB pathway activation and may be a promising drug in liver surgery to prevent HIRI.

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