Tetrachlorobenzoquinone exhibits neurotoxicity by inducing inflammatory responses through ROS-mediated IKK/IκB/NF-κB signaling

Fu, Juanli; Shi, Qiong; Song, Xiufang; Xia, Xiaomin; Su, Chuanyang; Liu, Zixuan; Song, Erqun; Song, Yang

doi:10.1016/j.etap.2015.12.012

Cited by 36 publications

(24 citation statements)

References 64 publications

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“…Inactive NF-κB combines with IκB, and is present in the cytoplasm. The IKKα complex, which induces the phosphorylation of IκB and NF-κB, translocates to the nucleus and regulates the transcription of iNOS and COX-2 [18,58]. LPS stimulation remarkably increases the phosphorylation of IKKα, with an equivalent increase in the phosphorylation and degradation of IκB [59].…”

Section: Discussionmentioning

confidence: 99%

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Bioconversion ofGentiana scabraBunge increases the anti-inflammatory effect in RAW 264.7 cells via MAP kinases and NF-κB pathway

Kim

Lee

Chon

et al. 2019

JABC

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Mitogen-activated protein (MAP) kinases play an important role in cell growth and differentiation, as well as the modulation of proinflammatory cytokines. The objective of this study was to examine the increase in the anti-inflammatory effect of Gentiana scabra Bunge (GSB), due to bioconversion with the Aspergillus kawachii crude enzyme, via inhibition of the NF-κB signaling and MAP kinase pathways in RAW 264.7 cells. The expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 in RAW 264.7 cells treated with the GSB ethyl acetate fraction bioconverted with A. kawachii crude enzyme (GE-BA), was dramatically suppressed as compared to GSB ethyl acetate fraction non-bioconverted with the A. kawachii crude enzyme (GE-UA). The phosphorylation of p38, extracellular signalregulated kinases, and inhibitory κB in RAW 264.7 cells treated with GE-BA was further suppressed, as compared to exposure to GE-UA. Moreover, the mRNA expression of interleukin 6, interleukin 1-beta, and tumor necrosis factor-α was further suppressed by GE-BA, compared to GE-UA. Similarly, antioxidant activities, such as 2,2-diphenyl-1-picrylhydrazyl hydrate and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) radical scavenging activity, of GE-BA were further increased compared to GE-UA. These observations demonstrate that the anti-oxidant and anti-inflammatory activities of GSB ethyl acetate fraction increases as a result from bioconversion with the A. kawachii crude enzyme.

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Section: Discussionmentioning

confidence: 99%

“…MAP kinases are activated by oxidative stress [16,17]. In addition, NF-κB is a relevant transcription regulator of inflammatory genes associated with many diseases [18]. Thus, the intake of bioactive substances with anti-oxidant properties could play important roles in various human diseases.…”

Section: Introductionmentioning

confidence: 99%

Bioconversion ofGentiana scabraBunge increases the anti-inflammatory effect in RAW 264.7 cells via MAP kinases and NF-κB pathway

Kim

Lee

Chon

et al. 2019

JABC

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“…(4) ROS acting as the upstream molecule of NF-κB, also affects IKK-NF-κB pathway [ 30 ]. Previous work showed that IKK expression and NF-κB secretion can increase rheumatoid arthritis synovial fibroblasts apoptosis by improving the level of IL-6 and CD147 [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

“…Apoptosis signaling kinase-1 [ 19 ], protein kinase C (PKC) [ 20 ], ERK [ 21 ], p53 [ 22 ], IkB kinase (IKK) [ 23 ], mitogen-activated protein kinase kinase (MEKK-1) [ 24 ], JNK [ 25 ], caspase-3 [ 26 ] and nuclear factor NF-κB [ 27 ] are associated with oxygen homeostasis and ischemic injury. All of them are associated with ROS-mediated pathways [ 28 , 29 , 30 , 31 ], whereas the overexpression of STC-1 has been reported to inhibit ROS production [ 32 ]. Furthermore, phosphate-modification plays an important role in the most molecules.…”

Section: Introductionmentioning

confidence: 99%

Stanniocalcin-1 Protects a Mouse Model from Renal Ischemia-Reperfusion Injury by Affecting ROS-Mediated Multiple Signaling Pathways

Liu

Shang

Liu

2016

IJMS

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Stanniocalcin-1 (STC-1) protects against renal ischemia-reperfusion injury (RIRI). However, the molecular mechanisms remain widely unknown. STC-1 inhibits reactive oxygen species (ROS), whereas most ROS-mediated pathways are associated with ischemic injury. Therefore, to explore the mechanism, the effects of STC-1 on ROS-medicated pathways were studied. Non-traumatic vascular clamps were used to establish RIRI mouse models. The serum levels of STC-1, interleukin-6 (IL-6), interferon (IFN) γ, P53, and capase-3 were measured by ELISA kits. Superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by fluorescence spectrofluorometer. All these molecules changed significantly in a RIRI model mouse when compared with those in a sham control. Kidney cells were isolated from sham and model mice. STC-1 was overexpressed or knockout in these kidney cells. The molecules in ROS-medicated pathways were measured by real-time quantitative PCR and Western blot. The results showed that STC-1 is an effective ROS scavenger. The serum levels of STC-1, MDA and SOD activity were increased while the serum levels of IL-6, iIFN-γ, P53, and capase-3 were decreased in a model group when compared with a sham control (p < 0.05). Furthermore, the levels of STC-1,p53, phosphorylated mitogen-activated protein kinase kinase (p-MEKK-1), c-Jun N-terminal kinase (p-JNK), extracellular signal-regulated kinase (p-ERK), IkB kinase (p-IKK), nuclear factor (NF) κB, apoptosis signal-regulating kinase 1 (ASK-1) and caspase-3 changed significantly in kidney cells isolated from a RIRI model when compared to those isolated from a sham control (p < 0.05). Meanwhile, STC-1 overexpression or silence caused significant changes of the levels of these ROS-mediated molecules. Therefore, STC-1 maybe improve anti-inflammation, anti-oxidant and anti-apoptosis activities by affecting ROS-mediated pathways, especially the phospho-modifications of the respective proteins, resulting in the increase of SOD and reduce of capase-3, p53, IL-6 and IFN-γ.

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“…In the recent years, NF‐κB signaling was reported to regulate neuronal process outgrowth (Gutierrez et al, ). The activation of NF‐κB involves the phosphorylation of inhibitor of nuclear factor kappa‐B kinase (IKK), which phosphorylates an inhibitor of NF‐κB (IκB), leading to sequent ubiquitination and degradation of IκB and the translocation of NF‐κB into the nucleus (Fu et al, ). Then NF‐κB regulates the transcription of NF‐κB target genes such as microtubule‐associated protein 1B (MAP1B) (Li et al, ).…”

Section: Introductionmentioning

confidence: 99%

Maternal marginal iodine deficiency limits dendritic growth of cerebellar purkinje cells in rat offspring by NF‐κB signaling and MAP1B

Dong

Wang

et al. 2016

Environmental Toxicology

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Iodine deficiency (ID) during early pregnancy had an adverse effect on children's psychomotor and motor function. It is worth noting that maternal marginal ID tends to be a common public health problem. Whether marginal ID potentially had adverse effects on the development of cerebellum and the underlying mechanisms remain unclear. Therefore, our aim was to study the effects of marginal ID on the dendritic growth in filial cerebellar Purkinje cells (PCs) and the underlying mechanism. In the present study, we established Wistar rat models by feeding dam rats with a diet deficient in iodine and deionized water supplemented with potassium iodide. We examined the total dendritic length using immunofluorescence, and Western blot analysis was conducted to investigate the activity of nuclear factor-κB (NF-κB) signaling and microtubule-associated protein 1B (MAP1B). Our results showed that marginal ID reduced the total dendritic length of cerebellar PCs, slightly down-regulated the activity of NF-κB signaling and decreased MAP1B in cerebellar PCs on postnatal day (PN) 7, PN14, and PN21. Our study may support the hypothesis that decreased T induced by marginal ID limits PCs dendritic growth, which may involve in the disturbance of NF-κB signaling and MAP1B on the cerebellum. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1241-1251, 2017.

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Tetrachlorobenzoquinone exhibits neurotoxicity by inducing inflammatory responses through ROS-mediated IKK/IκB/NF-κB signaling

Cited by 36 publications

References 64 publications

Bioconversion ofGentiana scabraBunge increases the anti-inflammatory effect in RAW 264.7 cells via MAP kinases and NF-κB pathway

Bioconversion ofGentiana scabraBunge increases the anti-inflammatory effect in RAW 264.7 cells via MAP kinases and NF-κB pathway

Stanniocalcin-1 Protects a Mouse Model from Renal Ischemia-Reperfusion Injury by Affecting ROS-Mediated Multiple Signaling Pathways

Maternal marginal iodine deficiency limits dendritic growth of cerebellar purkinje cells in rat offspring by NF‐κB signaling and MAP1B

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