ArticlePloS one2014
Long-time treatment by low-dose N-acetyl-L-cysteine enhances proinflammatory cytokine expressions in LPS-stimulated macrophages.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Lysosomes finely control macrophage inflammatory function via regulating the release of lysosomal FeNature communications · 2025Article
- Extraintestinal Manifestations in Induced Colitis: Controversial Effects ofOxidative medicine and cellular longevity · 2023Article
- Effects of N-acetyl cysteine on mitochondrial ROS, mitochondrial dynamics, and inflammation on lipopolysaccharide-treated human apical papilla cells.Clinical oral investigations · 2021Article
- Intracellular Redox-Modulated Pathways as Targets for Effective Approaches in the Treatment of Viral Infection.International journal of molecular sciences · 2021Review
- Effects of N-Acetylcysteine on the reproductive performance, oxidative stress and RNA sequencing of Nubian goats.Veterinary medicine and science · 2021Article
- Article
- Time-dependent C5a and C5aR expression in dental pulp cells following stimulation with LTA and LPS.International journal of molecular medicine · 2019Article
- Boosting GSH Using the Co-Drug Approach: I-152, a Conjugate ofNutrients · 2019Review
- IL-1 beta-mediated macrophage-hepatocyte crosstalk upregulates hepcidin under physiological low oxygen levels.Redox biology · 2019Article
- Saccharum Alhagi polysaccharide-1 and -2 promote the immunocompetence of RAW264.7 macrophagesExperimental and therapeutic medicine · 2018Article
- Biological Activities and Potential Oral Applications of N-Acetylcysteine: Progress and Prospects.Oxidative medicine and cellular longevity · 2018Review
- Lipopolysaccharide-Induced Nitric Oxide, Prostaglandin E2, and Cytokine Production of Mouse and Human Macrophages Are Suppressed by Pheophytin-b.International journal of molecular sciences · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-acetyl-L-cysteine is known to act as a reactive oxygen species scavenger and used in clinical applications. Previous reports have shown that high-dose N-acetyl-L-cysteine treatment inhibits the expression of proinflammatory cytokines in activated macrophages. Here, we have found that long-time N-acetyl-L-cysteine treatment at low-concentration increases phosphorylation of extracellular signal-regulated kinase 1/2 and AKT, which are essential for the induction of proinflammatory cytokines including interleukin 1β and interleukin 6 in lipopolysaccharide-stimulated RAW264.7 cells. Furthermore, long-time N-acetyl-L-cysteine treatment decreases expressions of protein phosphatases, catalytic subunit of protein phosphatase-2A and dual specificity phosphatase 1. On the other hand, we have found that short-time N-acetyl-L-cysteine treatment at low dose increases p53 expression, which inhibits expressions of proinflammatory cytokines. These observations suggest that long-time low-dose N-acetyl-L-cysteine treatment increases expressions of proinflammatory cytokines through enhancement of kinase phosphorylation.
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