Pentoxifylline prevents concanavalin A-induced hepatitis by reducing tumor necrosis factor α levels and inhibiting adhesion of T lymphocytes to extracellular matrix

Shirin, Haim; Bruck, Rafael; Aeed, Hussein; Frenkel, Daniela; Kenet, G.; Zaidel, Liliana; Avni, Yona; Halpern, Zamir; Hershkoviz, Rami

doi:10.1016/s0168-8278(98)80179-7

Cited by 23 publications

(17 citation statements)

References 30 publications

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“…NF-κB activation was associated with the phosphorylation and degradation of IκB-α [38,39]. Previous studies, showed that ginger root and its main poly-phenolic constituents (gingerols and zerumbone) exhibit anti-inflammatory effects in several cell types through the inhibition of the transcription factor NF-κB [40]. Our results demonstrate that the GE significantly reduced gene expression of NF-κB and induced marked upregulation of IκB.…”

Section: Discussionsupporting

confidence: 57%

Protective Effect of Zingiber Officinale against CCl4-Induced Liver Fibrosis Is Mediated through Downregulating the TGF-ß1/Smad3 and NF-κB/IκB Pathways

et al. 2015

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No ideal hepatoprotective agents are available in modern medicine to effectively prevent liver disorders. In this study, we aimed at evaluating the potential of Zingiber officinale in the regression of liver fibrosis and its underlining mechanism of action. To induce liver fibrosis, male Wistar rats received CCl₄ (2 ml/kg/2 times/week; i.p.), with and without 300 or 600 mg/kg Z. officinale extract daily through oral gavage. To assess the protective effect of Z. officinale, liver function parameters, histopathology, inflammatory markers and gene expression of transforming growth factor-beta 1 (TGF-ß1)/Smad3 and nuclear factor-kappa B (NF-ĸB)/IĸB pathways were analyzed. Results demonstrate that Z. officinale extract markedly prevented liver injury as evident by the decreased liver marker enzymes. Concurrent administration of Z. officinale significantly protected against the CCl₄-induced inflammation as showed by the decreased pro-inflammatory cytokine levels as well as the downregulation of the NF-κB/IκB and TGF-ß1/Smad3 pathways in CCl₄-administered rats. In conclusion, our study provides evidence that the protective effect of Z. officinale against rat liver fibrosis could be explained through its ability to modulate the TGF-ß1/Smad3 and NF-κB/IκB signaling pathways.

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Section: Discussionsupporting

confidence: 57%

Protective Effect of Zingiber Officinale against CCl4-Induced Liver Fibrosis Is Mediated through Downregulating the TGF-ß1/Smad3 and NF-κB/IκB Pathways

et al. 2015

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“…Consistent with these findings, liver histology in the mice treated with the free-radical scavengers was significantly improved. The time course of TNFa increase in Con A hepatitis has been documented in numerous previous studies including our own that described this model [1,2,[5][6][7][8]. The peak of TNFa elevation is 2 h after Con A injection and thereafter TNFa levels demonstrate a steady decline, thus the determination of TNFa levels in multiple time points is not essential.…”

Section: Discussionmentioning

confidence: 74%

“…Liver injury in this model occurs following the production of lymphokines and monokines such as tumor necrosis factor alpha (TNFa), interferon gamma (INFc), interleukin-6 (IL-6), and IL-1 [1][2][3][4][5]. The T-cell-induced apoptotic liver injury has been prevented by polyclonal TNFa antiserum [6], pretreatment with soluble receptor of TNFa [7], and pentoxifylline [8], indicating that the liver damage is mediated primarily by TNFa. On the other hand, protective effect of certain cytokines such as IL-6, IL-10, and IL-8 was also demonstrated [6,9].…”

Section: Introductionmentioning

confidence: 98%

Inhibition of Immune-Mediated Concanavalin A-Induced Liver Damage by Free-Radical Scavengers

et al. 2009

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“…However, there is extensive literature supporting its role as a potent immunomodulator such as decreases the synthesis of thromboxane B 2 (TXB 2 ), tumor necrosis factor-· (TNF-·), and cytokines (IL-1ß, IL-2, IL-6), and interferon-Á (IFN-Á) [11][12][13][14][15]. It has also been shown to diminish the degranulation, adherence, and superoxide generation by stimulated neutrophils [16][17][18][19]. The therapeutic benefits of the anti-inflammatory effects of PTXF have been demonstrated in several animal models as well as human cases of sepsis.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Pentoxifylline on Volume-Induced Lung Injury in Newborn Piglets

Smalling¹,

Suguihara²,

Huang³

et al. 2004

Neonatology

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To evaluate the efficacy of pentoxifylline (PTXF) in the attenuation of lung inflammation during volume-induced lung injury (VILI) in newborn piglets, 17 newborn piglets were mechanically ventilated with a large tidal volume (50 ml/kg) for a period of 8 h. They were randomly assigned to a placebo (PL, n = 9) or a treatment group (PTXF, n = 8) that received PTXF (20 mg/kg as a bolus, followed by a continuous infusion of 5 mg/kg/h). Hemodynamics, lung mechanics and arterial blood gases were measured during the 8 h of study. Serum and tracheoalveolar fluid (TAF) platelet-activating factor (PAF) and thromboxane (TXB₂) levels were obtained at baseline and at 8 h, while lung tissue myeloperoxidase (MPO) and wet to dry weight were assessed after the completion of the study. In the PL group, a marked increase in TAF PAF and TXB₂ levels was observed only in TAF, suggesting that the inflammatory process was localized within the lungs. A significant decrease in lung tissue MPO activity (p < 0.005) and lung wet to dry weight ratio (p < 0.04) was observed in the PTXF group. There were no differences in hemodynamics, arterial blood gases or lung mechanics measurements between groups. A significant reduction in pulmonary inflammatory response was observed during VILI in the PTXF pretreated animals. These results suggest that PTXF may be effective in modulating lung inflammation associated with mechanical ventilation in neonates.

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Pentoxifylline prevents concanavalin A-induced hepatitis by reducing tumor necrosis factor α levels and inhibiting adhesion of T lymphocytes to extracellular matrix

Cited by 23 publications

References 30 publications

Protective Effect of <b><i>Zingiber Officinale</i></b> against CCl<sub>4</sub>-Induced Liver Fibrosis Is Mediated through Downregulating the TGF-ß1/Smad3 and NF-κB/IκB Pathways

Protective Effect of <b><i>Zingiber Officinale</i></b> against CCl<sub>4</sub>-Induced Liver Fibrosis Is Mediated through Downregulating the TGF-ß1/Smad3 and NF-κB/IκB Pathways

Inhibition of Immune-Mediated Concanavalin A-Induced Liver Damage by Free-Radical Scavengers

Protective Effect of Pentoxifylline on Volume-Induced Lung Injury in Newborn Piglets

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Pentoxifylline prevents concanavalin A-induced hepatitis by reducing tumor necrosis factor α levels and inhibiting adhesion of T lymphocytes to extracellular matrix

Cited by 23 publications

References 30 publications

Protective Effect of <b><i>Zingiber Officinale</i></b> against CCl<sub>4</sub>-Induced Liver Fibrosis Is Mediated through Downregulating the TGF-ß1/Smad3 and NF-&#954;B/I&#954;B Pathways

Protective Effect of <b><i>Zingiber Officinale</i></b> against CCl<sub>4</sub>-Induced Liver Fibrosis Is Mediated through Downregulating the TGF-ß1/Smad3 and NF-&#954;B/I&#954;B Pathways

Inhibition of Immune-Mediated Concanavalin A-Induced Liver Damage by Free-Radical Scavengers

Protective Effect of Pentoxifylline on Volume-Induced Lung Injury in Newborn Piglets

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Protective Effect of <b><i>Zingiber Officinale</i></b> against CCl<sub>4</sub>-Induced Liver Fibrosis Is Mediated through Downregulating the TGF-ß1/Smad3 and NF-κB/IκB Pathways

Protective Effect of <b><i>Zingiber Officinale</i></b> against CCl<sub>4</sub>-Induced Liver Fibrosis Is Mediated through Downregulating the TGF-ß1/Smad3 and NF-κB/IκB Pathways