The Effect of Intraportal Prostaglandin E1 on Adhesion Molecule Expression, Inflammatory Modulator Function, and Histology in Canine Hepatic Ischemia/Reperfusion Injury

Hafez, T. S.; Moussa, Mona; Nesim, I.G.; Baligh, Nadia; Davidson, Brian R; Abdulhadi, Ahmad Salih

doi:10.1016/j.jss.2006.05.009

Cited by 38 publications

(35 citation statements)

References 48 publications

(62 reference statements)

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“…23,42 FD attenuated the H/R-induced HSP27 expression in SS mice compared to SS-SD animals ( Figure 5E, Online Supplementary Figure S6B), supporting the antiinflammatory effects of ω-3 PUFA following H/R stress. These findings align with data from other models of H/R liver injury 35,43 and confirm that VCAM-1 mediates adhesion events in the hepatic microvasculature and contributes to amplified inflammatory liver disease in SCD mice. In livers from SS mice, FD prevented vascular activation and reduced inflammation, improving endothelial dysfunction and reducing organ damage.…”

Section: E a B D C Fsupporting

confidence: 88%

Dietary -3 fatty acids protect against vasculopathy in a transgenic mouse model of sickle cell disease

et al. 2015

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The anemia of sickle cell disease is associated with a severe inflammatory vasculopathy and endothelial dysfunction, which leads to painful and life-threatening clinical complications. Growing evidence supports the anti-inflammatory properties of ω-3 fatty acids in clinical models of endothelial dysfunction. Promising but limited studies show potential therapeutic effects of ω-3 fatty acid supplementation in sickle cell disease. Here, we treated humanized healthy and sickle cell mice for 6 weeks with ω-3 fatty acid diet (fish-oil diet). We found that a ω-3 fatty acid diet: (i) normalizes red cell membrane ω-6/ ω-3 ratio; (ii) reduces neutrophil count; (iii) decreases endothelial activation by targeting endothelin-1 and (iv) improves left ventricular outflow tract dimensions. In a hypoxia-reoxygenation model of acute vaso-occlusive crisis, a ω-3 fatty acid diet reduced systemic and local inflammation and protected against sickle cell-related end-organ injury. Using isolated aortas from sickle cell mice exposed to hypoxia-reoxygenation, we demonstrated a direct impact of a ω-3 fatty acid diet on vascular activation, inflammation, and anti-oxidant systems. Our data provide the rationale for ω-3 dietary supplementation as a therapeutic intervention to reduce vascular dysfunction in sickle cell disease. ABSTRACTmice. 16,17 The animal protocol was approved by the Animal Care and Use Committee of the University of Verona (CIRSAL). Twomonth old animals were fed for 6 weeks with either the standard AIN-93M purified rodent diet (soy-diet with n6/n3 ratio of 8:1 -Dyets Inc., Bethlehem, PA, USA), containing 140 g/kg casein, 1.8 g/kg L-cystine, 100 g/kg sucrose, 465.9 g/kg cornstarch, 155 g/kg dextrose, 40 g/kg soybean oil, 0.8 mg/kg t-butylhydroquinone, 50 g/kg cellulose, 35 g/kg mineral mix, 10 g/kg vitamin mix, and 2.5 g/kg choline bitartrate 18 or the ω-3 FD, an AIN-93M-based purified rodent diet in which all of the calories provided by fat (10%) are replaced by 7.9% from HCO and 2.1% from ω-3 oil (Dyets Inc., Bethlehem, PA, USA). At the end of the 6 weeks of FD supplementation, animals were anesthetized with isofluorane, and whole blood was collected from each mouse via retro-orbital venipuncture by heparinized microcapillaries. Mice were euthanized and organs removed immediately. The organs were divided into two and either frozen immediately in liquid nitrogen or fixed in 10% formalin and embedded in paraffin for histology. Whenever indicated, 6-week old mice were exposed to hypoxia (8% oxygen for 10 h) followed by 3 h of reoxygenation (21% oxygen) (H/R stress) to mimic an acute VOC, as previously described.

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Section: E a B D C Fsupporting

confidence: 88%

Dietary -3 fatty acids protect against vasculopathy in a transgenic mouse model of sickle cell disease

et al. 2015

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“…Under the stress of I/R, the adhesion, rolling, and migration of leukocytes is induced through the upregulation of adhesion molecules in both leukocytes and sinusoidal endothelial cells (30). The ICAM and VCAM molecules are representative adhesion molecules that are upregulated on endothelial cells following I/R stress (8). As demonstrated in this study, BCAA treatment significantly attenuated the upregulation of ICAM and VCAM following I/R.…”

Section: Discussionsupporting

confidence: 64%

Protective effects of branched-chain amino acids on hepatic ischemia-reperfusion-induced liver injury in rats: a direct attenuation of Kupffer cell activation

Kitagawa

Yokoyama

Kokuryo

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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We determined whether there is a protective effect of branched-chain amino acid (BCAA) on hepatic ischemia-reperfusion (I/R)-induced acute liver injury. Wister rats were divided into the following four groups: simple laparotomy with vehicle; simple laparotomy with BCAA (1 g/kg body wt orally); I/R (30 min clamp) with vehicle; and I/R with BCAA. Serum liver function tests and the gene expression of adhesion molecules (intercellular adhesion molecule and vascular cell adhesion molecule) and vasoconstrictor-related genes (endothelin-1) in the liver were examined. In the in vivo study, portal venous pressure, leukocyte adhesion, and hepatic microcirculation were evaluated. Furthermore, Kupffer cells were isolated and cultured with various concentrations of BCAA in the presence or absence of lipopolysaccharide (LPS). Increased levels of liver function tests following I/R were significantly attenuated by BCAA treatment. The increased expression of adhesion molecules and endothelin-1 was also significantly attenuated by BCAA treatment. Moreover, increased portal venous pressure, enhanced leukocyte adhesion, and deteriorated hepatic microcirculation following I/R were all improved by BCAA treatment. In the experiment using isolated Kupffer cells, the expression of interleukin-6, interleukin-1β, and endothelin-1 in response to LPS stimulation was attenuated by BCAA in a dose-dependent fashion. These results indicate that perioperative oral administration of BCAA has excellent therapeutic potential to reduce I/R-induced liver injury. These beneficial effects may result from the direct attenuation of Kupffer cell activation under stressful conditions.

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“…On the other hand, iodized olive oil was also used as a drug carrier for PGE1, thereby increasing the drug concentration in the blood supply to the damaged liver artery (Idee and Guiu 2013). PGE1 protected the liver from, for example, fibrosis through a variety of ways that included inhibiting the immune response, preventing necrosis and the degeneration of liver cells, promoting the regeneration of liver cells, and improving hepatic microcirculation (Hanazaki et al 1999;Hafez et al 2007;Zou et al 2007). As part of the process, PGE1 was gradually released in the embolized area, where it reduced lipid peroxidation and oxidative damage through activating the oxidative stress defense system (Otogawa et al 2007;Jia et al 2013).…”

Section: Figmentioning

confidence: 99%

Preventative effects of prostaglandin E1 in combination with iodized olive oil on liver fibrosis after transcatheter arterial chemoembolization in a rabbit model of CCl₄-induced liver fibrosis

Jin

Cao

Wang

et al. 2015

Can. J. Physiol. Pharmacol.

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To explore the preventative effects of prostaglandin E1 (PGE1) on a rabbit model of CCl4-induced liver fibrosis after transcatheter arterial chemoembolization (TACE), we generated a rabbit model of CCl4-induced liver fibrosis by treatment with 40% CCl4 in iodized olive oil for 16 weeks. Body mass and serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total protein (TP), albumin (ALB), albumin:globulin ratio (A:G), total bilirubin (TBIL), and direct bilirubin (DBIL) were measured. After TACE, the levels of hyaluronic acid (HA), procollagen III (PC III), laminin (LN), and collagen IV (IV-C) were measured, and the severity of liver fibrosis as well as the morphology of liver tissues were determined. Body mass in the model group was significantly decreased from 10 to 16 weeks, and the serum levels of ALT, AST, TP, TBIL, and DBIL levels were significantly increased while the model was being generated; the levels of ALB and A:G were significantly decreased. After TACE, serum levels of HA, PC III, and LN in the group injected with 1.0 mL iodized olive oil (Group B) were higher than in the group that were injected with 1.0 mL iodized olive oil + 0.2 mL PGE1 (Group C), whereas the serum levels of IV-C were lower. The severity of liver fibrosis was ameliorated in Group C. The combination of PGE1 and iodized olive oil prevented the development of liver fibrosis following TACE.

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The Effect of Intraportal Prostaglandin E1 on Adhesion Molecule Expression, Inflammatory Modulator Function, and Histology in Canine Hepatic Ischemia/Reperfusion Injury

Cited by 38 publications

References 48 publications

Dietary -3 fatty acids protect against vasculopathy in a transgenic mouse model of sickle cell disease

Dietary -3 fatty acids protect against vasculopathy in a transgenic mouse model of sickle cell disease

Protective effects of branched-chain amino acids on hepatic ischemia-reperfusion-induced liver injury in rats: a direct attenuation of Kupffer cell activation

Preventative effects of prostaglandin E1 in combination with iodized olive oil on liver fibrosis after transcatheter arterial chemoembolization in a rabbit model of CCl₄-induced liver fibrosis

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The Effect of Intraportal Prostaglandin E1 on Adhesion Molecule Expression, Inflammatory Modulator Function, and Histology in Canine Hepatic Ischemia/Reperfusion Injury

Cited by 38 publications

References 48 publications

Dietary -3 fatty acids protect against vasculopathy in a transgenic mouse model of sickle cell disease

Dietary -3 fatty acids protect against vasculopathy in a transgenic mouse model of sickle cell disease

Protective effects of branched-chain amino acids on hepatic ischemia-reperfusion-induced liver injury in rats: a direct attenuation of Kupffer cell activation

Preventative effects of prostaglandin E1 in combination with iodized olive oil on liver fibrosis after transcatheter arterial chemoembolization in a rabbit model of CCl4-induced liver fibrosis

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Preventative effects of prostaglandin E1 in combination with iodized olive oil on liver fibrosis after transcatheter arterial chemoembolization in a rabbit model of CCl₄-induced liver fibrosis