Depletion of Kupffer cell function by gadolinium chloride attenuates thioacetamide-induced hepatotoxicity

Andrés, David; Sánchez-Reus, Isabel; Bautista, Mirandeli; Cascales, Marı́a

doi:10.1016/s0006-2952(03)00443-x

Cited by 77 publications

(55 citation statements)

References 39 publications

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“…Kupffer cell function by gadolinium chloride attenuates TAinduced hepatotoxicity (Andres et al, 2003). In the present study, TA-induced NF-B activation and liver injury was effectively inhibited by Man-or Suc-catalase, both of which are derivatives targeting Kupffer cells and liver endothelial cells through the recognition by mannose receptors or scavenger receptors, respectively.…”

Section: Downloaded Fromsupporting

confidence: 48%

Analysis of In Vivo Nuclear Factor-κB Activation during Liver Inflammation in Mice: Prevention by Catalase Delivery

Hyoudou¹,

Nishikawa²,

Kobayashi³

et al. 2006

Mol Pharmacol

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Nuclear factor-B (NF-B) is a transcription factor that plays crucial roles in inflammation, immunity, cell proliferation, and apoptosis. Until now, there have been few studies of NF-B activation in whole animals because of experimental difficulties. Here, we show that mice receiving a simple injection of plasmid vectors can be used to examine NF-B activation in the liver. Two plasmid vectors, pNF-B-Luc (firefly luciferase gene) and pRL-SV40 (Renilla reniformis luciferase gene), were injected into the tail vein of mice by the hydrodynamics-based procedure, an established method of gene transfer to mouse liver. Then, the ratio of the firefly and R. reniformis luciferase activities (F/R) was used as an indicator of the NF-B activity in the liver. Injection of thioacetamide or lipopolysaccharide plus D-galactosamine increased the F/R ratio in the liver, and this was significantly (P Ͻ 0.001) inhibited by an intravenous injection of catalase derivatives targeting liver nonparenchymal cells. Imaging the firefly luciferase expression in live mice clearly demonstrated that the catalase derivatives efficiently prevented the NF-B-mediated expression of the firefly luciferase gene. Plasma transaminases and the survival rate of mice supported the findings obtained by the luminescence-based analyses. Thus, this method, which requires no genetic recombination techniques, is highly sensitive to the activation of NF-B and allows us to continuously examine the activation in live animals. In conclusion, this novel, simple, and sensitive method can be used not only for analyzing the NF-B activation in the organ under different inflammatory conditions but also for screening drug candidates for the prevention of liver inflammation.

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Section: Downloaded Fromsupporting

confidence: 48%

Analysis of In Vivo Nuclear Factor-κB Activation during Liver Inflammation in Mice: Prevention by Catalase Delivery

Hyoudou¹,

Nishikawa²,

Kobayashi³

et al. 2006

Mol Pharmacol

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“…Evidence shows that depletion of Kupffer cell function attenuates TAA-induced hepatoxicity. 10,27) CD14/TLR4 is a component of the LPS receptor and has a key intermediary role in endotoxin-induced activation of Kupffer cells. 18) LBP enhances the binding of LPS to the CD14/TLR4 complex receptor on the Kupffer receptor, causing TNF-production.…”

Section: Discussionmentioning

confidence: 99%

A Standardized Aqueous Extract ofAnoectochilus formosanusAmeliorated Thioacetamide-Induced Liver Fibrosis in Mice: The Role of Kupffer Cells

Chuang

Yang

et al. 2010

Bioscience, Biotechnology, and Biochemistry

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“…In particular, this recruitment and activation of KCs, which are the resident macrophages of the liver, has been recognized as a major determinant for the extent of liver injury (Andrés et al, 2003;He et al, 2005;Kresse et al, 2005;Malaguarnera et al, 2006a). A positive correlation between the activity of KC and steatohepatitis, as well as activation of stellate cells, elevated TNF-␣ levels and lipid peroxidation in patients with both NASH and simple steatosis could be established (Malaguarnera et al, 2006b).…”

Section: Cross-talk Of Hepatocytes With Stellate Cells Fibroblasts mentioning

confidence: 99%

Molecular Mechanisms and Therapeutic Targets in Steatosis and Steatohepatitis

Anderson

Borlak²

2008

Pharmacol Rev

342

255

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Depletion of Kupffer cell function by gadolinium chloride attenuates thioacetamide-induced hepatotoxicity

Cited by 77 publications

References 39 publications

Analysis of In Vivo Nuclear Factor-κB Activation during Liver Inflammation in Mice: Prevention by Catalase Delivery

Analysis of In Vivo Nuclear Factor-κB Activation during Liver Inflammation in Mice: Prevention by Catalase Delivery

A Standardized Aqueous Extract ofAnoectochilus formosanusAmeliorated Thioacetamide-Induced Liver Fibrosis in Mice: The Role of Kupffer Cells

Molecular Mechanisms and Therapeutic Targets in Steatosis and Steatohepatitis

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