Immunohistochemical distribution of activated nuclear factor κB and peroxisome proliferator-activated receptors in carbon tetrachloride-induced chronic liver injury in rats

Orfila, C; Lepert, Jean-Claude; Alric, Laurent; Carrera, G.; Béraud, Maryse; Pipy, Bernard

doi:10.1007/s00418-005-0785-2

Cited by 37 publications

(30 citation statements)

References 41 publications

(40 reference statements)

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“…In the current investigation, immunohistochemical reactivity of both PPAR-α and PPAR-γ, increased in omega-3 supplemented rats compared to the only CCl 4 injected animals. Therefore, our results correlate the findings of previous studies [42,65,66] indicating CCl 4 treatment prominently reduce the expression of PPAR-γ, and that omega-3 supplementation has beneficial effects in reducing the development of degenerative changes induced by CCl 4 .…”

Section: Discussionsupporting

confidence: 92%

Salgı

Karaman¹,

Özen²,

Dağ³

et al. 2016

Kafkas Univ Vet Fak Derg

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Omega-3 is a polyunsaturated fatty acid known to have immunomodulatory functions. In the present study, ameliorative potential of omega-3 in experimental carbon tetrachloride (CCl4) toxicity was investigated. Total of 40 adult male Wistar albino rats were allocated into five groups and were subcutaneously given once every two days for 6 weeks the followings: Group 1 (Control): 0.5 ml/kg serum physiologic, Group 2 (Omega): 0.5 g/kg omega-3, Group 3 (Vehicle): 0.5 ml/kg pure olive oil, Group 4 (CCl4): 0.5 ml/kg CCl4, Group 5 (CCl4 + Omega): 0.5 ml/kg CCl4 plus 0.5 g/kg omega-3. At the end of the treatments, blood samples were collected and necropsy was performed for collection of liver tissues. Serum AST, AlT, GGT, TAC, TOC, triglyceride, and visfatin levels were detected. liver morphology and immunoreactivities against TGF-α, TGF-β, PPAR-α, and PPAR-γ were assessed. Serum AST, AlT, GGT, and TOC levels significantly increased while TAC level decreased in CCl4 given animals as compared to the control group. No significant changes were observed in triglyceride and visfatin levels. Immunohistochemical staining revealed increased TGF-α and TGF-β expressions and decreased PPAR-α and PPAR-γ expressions in liver of CCl4 given animals. Omega-3 supplementation has prominent effects in correcting the biochemical and immunohistochemical parameters studied as well as the tissue morphology. The results of the investigation indicated that omega-3 has ameliorative effects on the oxidative tissue degeneration and inflammatory processes induced by CCl4 treatment in rats. Keywords: CCl4, Omega-3, TGF-α, TGF-β, PPAR-α, PPAR-γ Karbon Tetraklorür Toksikasyonunda Omega-3'ün Koruyucu Etkisi ÖzetOmega-3 bağışıklığı düzenleyici fonksiyonları olduğu bilinen çoklu doymamış bir yağ asididir. Bu çalışmada, deneysel karbon tetraklorür (CCl4) toksikasyonunda omega-3'ün koruyucu potansiyel etkisi araştırılmıştır. Toplam 40 adet ergin erkek Wistar albino rat eşit beş gruba ayrıldı ve 6 hafta süresince her iki günde bir olmak üzere subkutan yolla deneklere tarif edilen uygulamalar yapıldı; Grup 1 (kontrol): 0.5 ml/kg serum fizyolojik, Grup 2 (Omega): 0.5 g/kg omega-3, Grup 3 (Taşıt): 0.5 ml/kg saf zeytin yağı, Grup 4 (CCl4): 0.5 ml/kg CCl4, Grup 5 (CCl4 + Omega): 0.5 ml/kg CCl4 artı 0.5 g/kg omega-3. Araştırma süresinin sonunda, kan örnekleri alınan deneklere karaciğer doku örneklerinin toplanması amacıyla nekropsi uygulandı. Serum AST, AlT, GGT, TAC, TOC, trigliserid ve visfatin seviyeleri belirlendi. Karaciğer morfolojisi incelendi ve TGF-α, TGF-β, PPAR-α ve PPAR-γ immunreaktiviteleri tespit edildi. Kontrol grubu ile karşılaştırıldığında CCl4 verilen hayvanlarda serum AST, AlT, GGT ve TOC seviyelerinin anlamlı derecede arttığı, TAC seviyesinin ise azaldığı gözlemlendi. Trigliserid ve visfatin seviyelerinde anlamlı bir değişikliğin olmadığı belirlendi. İmmunohistokimyasal boyamalarda CCl4 verilen hayvanlarda TGF-α ve TGF-β immunreaktiviteleri artarken PPAR-α ve PPAR-γ immunreaktivitelerinde azalma dikkati çekti. Omega-3 takviyesinin incel...

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Section: Discussionsupporting

confidence: 92%

Salgı

Karaman¹,

Özen²,

Dağ³

et al. 2016

Kafkas Univ Vet Fak Derg

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“…It is also known that the NFB and MAPK pathways, including p38 and JNK, participate in HSC activation [45,46,47]. Therefore, we treatment of rats, and ongoing production of proinflammatory cytokines regulated by NFB is believed to play a major role in CCl 4 -induced liver fibrosis [48,49,50]. The key feature of liver fibrosis is the increase in collagen type I synthesis.…”

Section: Discussionmentioning

confidence: 99%

Zinc supplementation attenuates ethanol- and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling

Szuster‐Ciesielska

Plewka

Daniluk

et al. 2009

Biochemical Pharmacology

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To cite this version:Agnieszka Szuster-Ciesielska, Krzysztof Plewka, Jadwiga Daniluk, Martyna Kandefer-Szerszeń. Zinc supplementation attenuates ethanol-and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling. Biochemical Pharmacology, Elsevier, 2009, 78 (3) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Specifically, the complex binds to promoter regions of a large number of genes involved in the inflammatory response, such as those encoding intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM), IL-1, TNF-␣, IL-6, and inducible nitric oxide synthase (18,25). NF-B binding activity was found to increase in liver macrophages and hepatocytes after CCl 4 treatment in rats (23), and ongoing production of inflammatory cytokines regulated by NF-B is believed to play a major role in CCl 4 -induced liver fibrosis (5,40).…”

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confidence: 99%

Selective inactivation of NF-κB in the liver using NF-κB decoy suppresses CCl₄-induced liver injury and fibrosis

Son¹,

Iimuro²,

Seki³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

115

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Sustained hepatic inflammation induced by various causes can lead to liver fibrosis. Transcription factor NF-κB is important in regulating inflammatory responses, especially in macrophages. We presently investigated whether an NF-κB decoy, a synthetic oligodeoxynucleotide (ODN) imitating the NF-κB binding site, inhibited the inflammatory response after CCl4 intoxication to prevent CCl4-induced hepatic injury and fibrosis. The NF-κB decoy was introduced into livers by injecting the spleens of mice, using a hemagglutinating virus of Japan (HVJ)-liposome method. ODN was transferred mainly to macrophages in normal or fibrotic livers. Increases in serum transaminases and production of inflammatory cytokines after a single challenge with CCl4 were inhibited by the NF-κB decoy, which suppressed nuclear translocation of NF-κB in liver macrophages. Liver fibrosis induced by CCl4 administration for 8 wk was suppressed by the NF-κB decoy, accompanied by diminished mRNA expression for transforming growth factor (TGF)-β, procollagen type 1 α1, and α-smooth muscle actin (SMA). In vitro, isolated liver macrophages showed increased DNA binding activity of NF-κB and inflammatory cytokine production after hydrogen peroxide treatment; both increases were inhibited significantly by the NF-κB decoy. In contrast, NF-κB decoy transferred to isolated hepatic stellate cells (HSC) had no effect on their morphological activation or α-SMA expression, although the decoy accelerated tumor necrosis factor (TNF)-α-induced apoptosis in activated HSC. The effect of NF-κB decoy suppressing fibrosis probably results mainly from anti-inflammatory effects on liver macrophages, with a possible minor contribution from its direct proapoptotic effect on activated HSC.

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Immunohistochemical distribution of activated nuclear factor κB and peroxisome proliferator-activated receptors in carbon tetrachloride-induced chronic liver injury in rats

Cited by 37 publications

References 41 publications

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Salgı

Zinc supplementation attenuates ethanol- and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling

Selective inactivation of NF-κB in the liver using NF-κB decoy suppresses CCl₄-induced liver injury and fibrosis

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Immunohistochemical distribution of activated nuclear factor κB and peroxisome proliferator-activated receptors in carbon tetrachloride-induced chronic liver injury in rats

Cited by 37 publications

References 41 publications

Salgı

Salgı

Zinc supplementation attenuates ethanol- and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling

Selective inactivation of NF-κB in the liver using NF-κB decoy suppresses CCl4-induced liver injury and fibrosis

Contact Info

Product

Resources

About

Selective inactivation of NF-κB in the liver using NF-κB decoy suppresses CCl₄-induced liver injury and fibrosis