Hepatoprotective Effect of Infliximab, an Anti-TNF-α Agent, on Carbon Tetrachloride-Induced Hepatic Fibrosis

Bahçecıoğlu, İbrahim Halil; Koca, Süleyman Serdar; Poyrazoğlu, Orhan Kürşat; Yalnız, Mehmet; Ozercan, İbrahim Hanifi; Üstündağ, Bilal; Şahin, Kazım; Dağlı, Adile Ferda; Işık, Ahmet Turan

doi:10.1007/s10753-008-9067-1

Cited by 62 publications

(58 citation statements)

References 33 publications

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“…CCl4 application was carried out intraperitoneally twice per week for four weeks at 1.5 mL/kg live weight injected together with olive oil at 1:3 ratio (Bahcecioglu et al, 2008;Shaker et al, 2010).…”

Section: Ccl4 Applicationmentioning

confidence: 99%

<i>Nigella sativa</i> improves the carbon tetrachloride-induced lung damage in rats through repression of erk/akt pathway

Aslan

Boydak

Can

et al. 2015

Bangladesh J Pharmacol

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The objective of this study was to examine whether Nigella sativa plays a protective role against the damage in the lung by administering carbon tetrachloride (CCl4) to rats. Male Wistar albino (n=28, 8 weeks old) rats were divided into 4 groups: a) negative control: Normal water consuming group to which no CCl4 and N. sativa was administered; b) Positive control: Normal water consuming group to which no CCl4 was administered but N. sativa was administered; c) CCl4 Group: Normal water consuming and group to which CCl4 was administered (1.5 mL/kg, ip); d) N. sativa plus CCl4 group: CCl4 and N. sativa administered group (1.5 mL/kg, ip). Caspase-3, caspase -9, erk, akt protein syntheses were examined via Western blotting. Malondialdehyde determination in lung tissue was made using spectrophotometer. As a results, malondialdehyde amount was decreased in the CCl4 plus N. sativa group in comparison to CCl4 group whereas caspase-3, caspase-9 was increased and erk, akt had decreased. These results show that N. sativa protects the lung against oxidative damage.

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Section: Ccl4 Applicationmentioning

confidence: 99%

<i>Nigella sativa</i> improves the carbon tetrachloride-induced lung damage in rats through repression of erk/akt pathway

Aslan

Boydak

Can

et al. 2015

Bangladesh J Pharmacol

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“…Because both IL-6 and TNF-α have pleiotropic effects on hepatic leukocytes in liver fibrosis (10,11), we postulated that DCs may be a central determinant of the inflammatory milieu in the fibrotic liver. To test this hypothesis, NPCs were harvested from normal and fibrotic livers and cultured for 24 hours without exogenous stimulation in parallel with NPCs from fibrotic livers that had been depleted of DCs.…”

Section: Introductionmentioning

confidence: 99%

In liver fibrosis, dendritic cells govern hepatic inflammation in mice via TNF-α

Connolly¹,

Bedrosian²,

Clair³

et al. 2009

J. Clin. Invest.

184

201

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Hepatic fibrosis occurs during most chronic liver diseases and is driven by inflammatory responses to injured tissue. Because DCs are central to modulating liver immunity, we postulated that altered DC function contributes to immunologic changes in hepatic fibrosis and affects the pathologic inflammatory milieu within the fibrotic liver. Using mouse models, we determined the contribution of DCs to altered hepatic immunity in fibrosis and investigated the role of DCs in modulating the inflammatory environment within the fibrotic liver. We found that DC depletion completely abrogated the elevated levels of many inflammatory mediators that are produced in the fibrotic liver. DCs represented approximately 25% of the fibrotic hepatic leukocytes and showed an elevated CD11b + CD8 -fraction, a lower B220 + plasmacytoid fraction, and increased expression of MHC II and CD40. Moreover, after liver injury, DCs gained a marked capacity to induce hepatic stellate cells, NK cells, and T cells to mediate inflammation, proliferation, and production of potent immune responses. The proinflammatory and immunogenic effects of fibrotic DCs were contingent on their production of TNF-α. Therefore, modulating DC function may be an attractive approach to experimental therapeutics in fibro-inflammatory liver disease.

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“…When the treatment was changed with ETN or ADA, hepatotoxicity disappeared in some patients who received IFX previously [33,34]. On the other hand, TNFα blockage was associated with the hepatoprotective effect in some conditions in mice models [35,36]. Another study reported that IFX treatment can control chronic hepatitis C infections by promoting apoptotic cells and preventing liver regeneration in a transgenic mouse model [37].…”

Section: Discussionmentioning

confidence: 99%

Acute Brucella melitensis M16 infection model in mice treated with tumor necrosis factor-alpha inhibitors

Kutlu

Ergin

Şentürk

et al. 2015

J Infect Dev Ctries

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Introduction: There is limited data in the literature about brucellosis related to an intracellular pathogen and anti-tumor necrosis factor alpha (anti-TNFα) medication. The aim of this study was to evaluate acute Brucella infections in mice receiving anti-TNFα drug treatment. Methodology: Anti-TNFα drugs were injected in mice on the first and fifth days of the study, after which the mice were infected with B. melitensis M16 strain. Mice were sacrificed on the fourteenth day after infection. Bacterial loads in the liver and spleen were defined, and histopathological changes were evaluated. Results: Neither the liver nor the spleen showed an increased bacterial load in all anti-TNFα drug groups when compared to a non-treated, infected group. The most significant histopathological findings were neutrophil infiltrations in the red pulp of the spleen and apoptotic cells with hepatocellular pleomorphism in the liver. There was no significant difference among the groups in terms of previously reported histopathological findings, such as extramedullary hematopoiesis and granuloma formation. Conclusions: There were no differences in hepatic and splenic bacterial load and granuloma formation, which indicate worsening of the acute Brucella infection in mice; in other words, anti-TNFα treatment did not exacerbate the acute Brucella spp. infection in mice.

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Hepatoprotective Effect of Infliximab, an Anti-TNF-α Agent, on Carbon Tetrachloride-Induced Hepatic Fibrosis

Cited by 62 publications

References 33 publications

<i>Nigella sativa</i> improves the carbon tetrachloride-induced lung damage in rats through repression of erk/akt pathway

<i>Nigella sativa</i> improves the carbon tetrachloride-induced lung damage in rats through repression of erk/akt pathway

In liver fibrosis, dendritic cells govern hepatic inflammation in mice via TNF-α

Acute Brucella melitensis M16 infection model in mice treated with tumor necrosis factor-alpha inhibitors

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