ArticleYonago acta medica2016
Preconditioning by Low Dose LPS Prevents Subsequent LPS-Induced Severe Liver Injury via Nrf2 Activation in Mice.
Article in Yonago acta medica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
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- High-Intensity Exercise Prevents Disturbances in Lung Inflammatory Cytokines and Antioxidant Defenses Induced by Lipopolysaccharide.Inflammation · 2018Article
- Overexpression of homeodomain-interacting protein kinase 2 (HIPK2) attenuates sepsis-mediated liver injury by restoring autophagy.Cell death & disease · 2018Article
- Distribution and Neurochemistry of the Porcine Ileocaecal Valve Projecting Sensory Neurons in the Dorsal Root Ganglia and the Influence of Lipopolysaccharide from Different Serotypes ofInternational journal of molecular sciences · 2018Article
- Pretreatment of Low-Dose and Super-Low-Dose LPS on the Production ofToxicological research · 2018Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis is a syndrome triggered by endotoxin lipopolysaccharide (LPS) during bacterial infection. Sepsis sometimes recurs, with the second sepsis giving rise to a different phenotype because of disease modification by the preceding sepsis. Such a protective modification is called a preconditioning (PC) effect. PC is an endogenous protective mechanism by which sublethal damage confers tolerance to a subsequent lethal load. Oxidative stress is one of the important pathogenetic mechanisms that occur in sepsis. The nuclear factor erythroid 2 (NF-E2)-related factor-2 (Nrf2) system is a key regulatory transcription factor that protects organs and cells against oxidative stress and may be associated with the PC effect in repeated sepsis.
methodsThe effect of PC induced by low-dose LPS on survival rate and liver injury against subsequent high-dose LPS stimulation was examined using a mouse model of sepsis. In order to understand the detailed mechanism(s) involved in the PC effect within the liver, gene expression array was performed. As a candidate mechanism of PC, the activation of the Nrf2 system was analyzed using Nrf2 reporter mice. Furthermore, the induction of heme oxygenase-1 (HO-1), one of the main targets of Nrf2, in the liver was examined by immunoblotting and immunohistochemistry. The PC effect on liver injury induced by LPS was further examined using Nrf2-deficient mice.
resultsPC by LPS (1.7 or 5.0 mg/kg body weight, intraperitoneally) increased the survival rate of mice and decreased liver injury in response to a subsequent injection of a lethal level of LPS (20 mg/kg body weight). DNA array revealed that the gene ontology term "antioxidant activity" as one of the candidate mechanisms of the PC effect by LPS. In Nrf2 reporter mice, PC immediately and intensely enhanced luminescence that indicated Nrf2 activation after subsequent LPS injection. The induction of HO-1 by LPS was also enhanced by preceding PC, and its induction was observed mainly in Kupffer cells of the liver. In Nrf2-deficient mice, the induction of HO-1 in Kupffer cells and the hepatoprotective effect of PC were decreased as compared with wild-type mice.
conclusionOur results suggest that activation of the Nrf2 system is, at least in part, one of the mechanisms of a PC effect in the mouse liver in the case of repeated LPS stimulation.
Indexed as
Identifiers
27708538PMC5050272W2530746425What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.