ArticleOncotarget2015
Nickel chloride (NiCl2)-caused inflammatory responses via activation of NF-κB pathway and reduction of anti-inflammatory mediator expression in the kidney.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- The Protective Effects of Methionine on Nickel-Induced Oxidative Stress via NF-κB Pathway in the Kidneys of Mice.Biological trace element research · 2025Article
- Nickel-based nanomaterials: a comprehensive analysis of risk assessment, toxicity mechanisms, and future strategies for health risk prevention.Journal of nanobiotechnology · 2025Review
- Protective effects of gallic acid against nickel-induced kidney injury: impact of antioxidants and transcription factor on the incidence of nephrotoxicity.Renal failure · 2024Article
- Article
- Association between multiple-heavy-metal exposures and systemic immune inflammation in a middle-aged and elderly Chinese general population.BMC public health · 2024Article
- A gene expression biomarker for predictive toxicology to identify chemical modulators of NF-κB.PloS one · 2022Article
- Nickel carcinogenesis mechanism: cell cycle dysregulation.Environmental science and pollution research international · 2021Review
- Redox Homeostasis in Poultry: Regulatory Roles of NF-κB.Antioxidants (Basel, Switzerland) · 2021Review
- Update of the risk assessment of nickel in food and drinking water.EFSA journal. European Food Safety Authority · 2020Article
- Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives.Biomolecules · 2020Review
- Circular RNAs: epigenetic regulators in cancerous and noncancerous skin diseases.Cancer gene therapy · 2020Review
- Article
- Enhanced Biosorption of Nickel Ions on Immobilized Surface-Engineered Yeast Using Nickel-Binding Peptides.Frontiers in microbiology · 2019Article
- Environmental pollution and kidney diseases.Nature reviews. Nephrology · 2018Review
- Circular RNAs function as ceRNAs to regulate and control human cancer progression.Molecular cancer · 2018Review
- Arsenic and/or copper caused inflammatory response via activation of inducible nitric oxide synthase pathway and triggered heat shock protein responses in testis tissues of chicken.Environmental science and pollution research international · 2018Article
- HMGB1 Increases IL-1β Production in Vascular Smooth Muscle Cells via NLRP3 Inflammasome.Frontiers in physiology · 2018Article
- Role of calcium channels and endothelial factors in nickel induced aortic hypercontraction in Wistar rats.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2018Article
- Article
- Sodium fluoride induces renal inflammatory responses by activating NF-κB signaling pathway and reducing anti-inflammatory cytokine expression in mice.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nickel (Ni) or Ni compounds target a number of organs and produce multiple toxic effects. Kidney is the major organ for Ni accumulation and excretion. There are no investigations on the Ni- or Ni compounds-induced renal inflammatory responses in human beings and animals at present. Therefore, we determined NiCl2-caused alteration of inflammatory mediators, and functional damage in the broiler's kidney by the methods of biochemistry, immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR). Dietary NiCl2 in excess of 300 mg/kg caused the renal inflammatory responses that characterized by increasing mRNA expression levels of the pro-inflammatory mediators including tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8) and interleukin-18 (IL-18) via the activation of nucleic factor κB (NF-κB), and decreasing mRNA expression levels of the anti-inflammatory mediators including interleukin-2 (IL-2), interleukin-4 (IL-4) and interleukin-13 (IL-13). Concurrently, NiCl2 caused degeneration, necrosis and apoptosis of the tubular cells, which was consistent with the alteration of renal function parameters including elevated alkaline phosphatase (AKP) activity, and reduced activities of sodium-potassium adenosine triphosphatase (Na(+)/K(+)-ATPase), calcium adenosine triphosphatase (Ca(2+)-ATPase), lactic dehydrogenase (LDH), succinate dehydrogenase (SDH) and acid phosphatase (ACP) in the kidney. The above-mentioned results present that the activation of NF-κB pathway and reduction of anti-inflammatory mediator expression are main mechanisms of NiCl2-caused renal inflammatory responses and that the renal function is decreased or impaired after NiCl2-treated.
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