Research Papers: Immunology:
Sodium fluoride induces renal inflammatory responses by activating NF-κB signaling pathway and reducing anti-inflammatory cytokine expression in mice
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Qin Luo1, Hengmin Cui1,2, Huidan Deng1, Ping Kuang1, Huan Liu1, Yujiao Lu1, Jing Fang1,2, Zhicai Zuo1,2, Junliang Deng1,2, Yinglun Li1,2, Xun Wang1,2 and Ling Zhao1,2
1 College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China
2 Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu, China
Hengmin Cui, email:
Keywords: sodium fluoride, inflammatory responses, NF-κB, anti-inflammatory cytokines, kidney, Immunology and Microbiology Section, Immune response, Immunity
Received: April 28, 2017 Accepted: June 20, 2017 Published: July 05, 2017
Fluoride is widely distributed in the environment and often results in adverse health effects on animals and human beings. It has been proved that fluoride can induce inflammatory responses in vitro. However, very limited reports are focused on fluoride-induced inflammatory responses in vivo. In this study, mice were used to investigate sodium fluoride (NaF) induced renal inflammatory responses and the potential mechanism by using the methods of pathology, biochemistry, enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. A total of 240 ICR mice were randomly divided into four equal groups: the control group and three experimental groups (NaF was given orally at the dose of 0, 12, 24 and 48 mg/kg body weight for 42 days, respectively). The results showed that NaF in excess of 12 mg/kg induced the renal histopathological lesions, and inflammatory responses via the activation of nuclear factor-kappa B (NF-κB) signaling pathway and the reduction of anti-inflammatory cytokines expression. The activation of NF-κB signaling pathway was characterized by increasing the nitric oxide (NO) and prostaglandin E2 (PGE2) contents, inducible nitric oxide synthase (iNOS) activities and mRNA expression levels, and the mRNA and protein expression levels of cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and interleukin-8 (IL-8) in three NaF-treated groups. Concurrently, the mRNA and protein expression levels of the anti-inflammatory cytokines including interleukin-4 (IL-4) and interleukin-10 (IL-10) were decreased in three experimental groups when compared with those in the control group.
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