ArticleMolecular medicine reports2016
Inhibition of the translocation and extracellular release of high-mobility group box 1 alleviates liver damage in fibrotic mice in response to D-galactosamine/lipopolysaccharide challenge.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Hepatic galectin-3 is associated with lipid droplet area in non-alcoholic steatohepatitis in a new swine model.Scientific reports · 2022Article
- M2-like macrophages exert hepatoprotection in acute-on-chronic liver failure through inhibiting necroptosis-S100A9-necroinflammation axis.Cell death & disease · 2021Article
- Phenotypic switch of human and mouse macrophages and resultant effects on apoptosis resistance in hepatocytes.Innate immunity · 2019Article
- Cellular Mechanisms of Hepatoprotection Mediated by M2-Like Macrophages.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- M2-like macrophages in the fibrotic liver protect mice against lethal insults through conferring apoptosis resistance to hepatocytes.Scientific reports · 2017Article
- Gut Microbiome-Based Metagenomic Signature for Non-invasive Detection of Advanced Fibrosis in Human Nonalcoholic Fatty Liver Disease.Cell metabolism · 2017Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute liver injury in the setting of fibrosis is an area of interest in investigations, and remains to be fully elucidated. Previous studies have suggested the beneficial effects of liver fibrosis induced by thioacetamide and partial bile duct ligation against Fas‑mediated acute liver injury. The activation of AKT and extracellular signal-regulated kinase signaling is considered to be crucial in this hepatoprotection. To demonstrate the protection of CCl4‑induced liver fibrosis against lethal challenge, the present study compared the reactivity to lethal doses of D‑galactosamine (D-GalN)/lipopolysaccharide (LPS) between fibrotic mice and control mice groups. The extent of hepatic damage was assessed by survival rate and histopathological analysis. The molecular basis of the fibrosis‑based hepatoprotection was examined, with a particular focus on the translocation and release of high‑mobility group box (HMGB)1 and the inflammatory response triggered by HMGB1. Hepatoprotection induced by fibrosis was demonstrated by improved survival rates (100%, vs. 20%) and improved preservation of liver architecture in fibrotic mice subjected to D‑GalN/LPS, compared with control mice treated in the same way. D‑GalN/LPS evoked the translocation and release of HMGB1, detected by immunohistochemistry, in the control mice, which was significantly inhibited in the fibrotic mice. The gene expression levels of HMGB1‑associated proinflammatory cytokines, including interleukin (IL)‑1β, IL‑6, tumor necrosis factor‑α and IL‑12p40, were markedly inhibited in the fibrotic mice when exposed to D‑GalN/LPS. These findings confirmed that CCl4‑based fibrosis induced hepatoprotection, and provided evidence that fibrosis inhibited the translocation and release of HMGB1, and the proinflammatory response triggered by HMGB1. This alleviated liver damage following exposure to D‑GalN/LPS challenge.
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