title: Nickel chloride (NiCl2)-caused inflammatory responses via activation of NF-κB pathway and reduction of anti-inflammatory mediator expression in the kidney.
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.
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.
authors.forename: Hongrui
authors.initials: H
authors.lastname: Guo
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.
authors.forename: Huidan
authors.initials: H
authors.lastname: Deng
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.|College of Veterinary Medicine, Sichuan Agricultural University Ya'an, Sichuan, China.
authors.forename: Hengmin
authors.initials: H
authors.lastname: Cui
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.|College of Veterinary Medicine, Sichuan Agricultural University Ya'an, Sichuan, China.
authors.forename: Xi
authors.initials: X
authors.lastname: Peng
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.|College of Veterinary Medicine, Sichuan Agricultural University Ya'an, Sichuan, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Fang
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.|College of Veterinary Medicine, Sichuan Agricultural University Ya'an, Sichuan, China.
authors.forename: Zhicai
authors.initials: Z
authors.lastname: Zuo
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.|College of Veterinary Medicine, Sichuan Agricultural University Ya'an, Sichuan, China.
authors.forename: Junliang
authors.initials: J
authors.lastname: Deng
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.|College of Veterinary Medicine, Sichuan Agricultural University Ya'an, Sichuan, China.
authors.forename: Xun
authors.initials: X
authors.lastname: Wang
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.
authors.forename: Bangyuan
authors.initials: B
authors.lastname: Wu
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agricultural University, Ya'an, Sichuan, China.
authors.forename: Kejie
authors.initials: K
authors.lastname: Chen
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002645:Chickens; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D007249:Inflammation / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism*; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007673:Kidney Cortex Necrosis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D009532:Nickel / Q000378:metabolism / Q000633:toxicity*; D012333:RNA, Messenger / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013997:Time Factors
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D016328:NF-kappa B; D012333:RNA, Messenger; C022838:nickel chloride; D009532:Nickel
keywords: Immune response; Immunity; Immunology and Microbiology Section; NF-κB; NiCl; inflammation; kidney; mRNA expression