N,N-dimethylformamide-induced acute liver damage is driven by the activation of NLRP3 inflammasome in liver macrophages of mice

Liu, Hong; Li, Mingjun; Zhang, Xiu-Ning; Wang, Shuo; Li, Long-Xia; Guo, Fangfang; Zeng, Tao

doi:10.1016/j.ecoenv.2022.113609

Cited by 10 publications

(8 citation statements)

References 43 publications

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“…Liu’s team found that increased ROS can activate the p38 MAPK pathway and ultimately inhibit the anti-inflammatory phenotype of macrophages (Liu et al, 2022). In arsenic-induced mouse neurobehavioral disorders, the ROS/p38 MAPK/NLRP3 inflammasome cascade reaction was also observed (Liu et al, 2023). In the present study, we used NAC to inhibit the high level of ROS induced by nano MnO 2 in BV2 cells.…”

Section: Discussionmentioning

confidence: 99%

Manganese dioxide nanoparticles provoke inflammatory damage in BV2 microglial cells via increasing reactive oxygen species to activate the p38 MAPK pathway

Sun,

Qin,

Liang

et al. 2024

Toxicol Ind Health

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With the widespread use of manganese dioxide nanoparticles (nano MnO2), health hazards have also emerged. The inflammatory damage of brain tissues could result from nano MnO2, in which the underlying mechanism is still unclear. During this study, we aimed to investigate the role of ROS-mediated p38 MAPK pathway in nano MnO2-induced inflammatory response in BV2 microglial cells. The inflammatory injury model was established by treating BV2 cells with 2.5, 5.0, and 10.0 μg/mL nano MnO2 suspensions for 12 h. Then, the reactive oxygen species (ROS) scavenger (20 nM N-acetylcysteine, NAC) and the p38 MAPK pathway inhibitor (10 μM SB203580) were used to clarify the role of ROS and the p38 MAPK pathway in nano MnO2-induced inflammatory lesions in BV2 cells. The results indicated that nano MnO2 enhanced the expression of pro-inflammatory cytokines IL-1β and TNF-α, elevated intracellular ROS levels and activated the p38 MAPK pathway in BV2 cells. Controlling intracellular ROS levels with NAC inhibited p38 MAPK pathway activation and attenuated the inflammatory response induced by nano MnO2. Furthermore, inhibition of the p38 MAPK pathway with SB203580 led to a decrease in the production of inflammatory factors (IL-1β and TNF-α) in BV2 cells. In summary, nano MnO2 can induce inflammatory damage by increasing intracellular ROS levels and further activating the p38 MAPK pathway in BV2 microglial cells.

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Section: Discussionmentioning

confidence: 99%

Manganese dioxide nanoparticles provoke inflammatory damage in BV2 microglial cells via increasing reactive oxygen species to activate the p38 MAPK pathway

Sun,

Qin,

Liang

et al. 2024

Toxicol Ind Health

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“…The potential mechanism of targeted harmful effects of N,N -Dimethylformamide on liver was mainly contributed to oxidative stress caused by reduced GSH level and increased reactive oxygen species ( 51 ). And it was also found that the harmful mechanism of N,N -Dimethylformamide involved the activation of NLRP3 inflammasome ( 52 ), suggesting the induced inflammatory reaction may also be the underlying cause. The exposure to ethylbenzene, styrene was also reported to cause harmful effect on the central nervous, immune and reproductive systems ( 25 , 53 ), while its potential harmful cause of RA was firstly found in this study.…”

Section: Discussionmentioning

confidence: 99%

The exposure to volatile organic chemicals associates positively with rheumatoid arthritis: a cross-sectional study from the NHANES program

Lei

Yang

et al. 2023

Front. Immunol.

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IntroductionRheumatoid arthritis (RA) is an autoimmune disease and closely associated with both genetic and environmental factors. Volatile organic chemicals (VOC), a common environment pollutant, was associated with some autoimmune diseases, while whether VOC exposure or which VOC leads to RA is yet clarified.MethodsA cross-sectional study using data from the 6 survey cycles (2005-2006, 2011-2012, 2013-2014, 2015-2016, 2017-2018, 2017-2020) of NHANES program was performed. The RA or non-arthritis status of participant was identified through a questionnaire survey. The quantile logistic regression method was used for correlation analysis between VOC metabolites (VOCs) in urine and RA. The covariates included age, gender, race, educational level, marital status, total energy intake, physical activity, smoking, hypertension, diabetes, urine creatinine, albumin and marihuana use.ResultsA total of 9536 participants (aged 20 to 85) with 15 VOCs, comprising 618 RA and 8918 non-arthritis participants, was finally included for analysis. Participants in the RA group showed higher VOCs in urine than that in the non-arthritis group. A positive association between 2 VOCs (AMCC: Q4: OR=2.173, 95%CI: 1.021, 4.627. 3HPMA: Q2: OR=2.286, 95%CI: 1.207 - 4.330; Q4: OR=2.663, 95%CI: 1.288 -5.508.) and RA was detected in the model 3, which was independent of all the covariates. The relative parent compounds of the two VOCs included N,N-Dimethylformamide and acrolein.DiscussionThese findings suggested that the VOC exposure significantly associated with RA, providing newly epidemiological evidence for the establishment that environmental pollutants associated with RA. And also, more prospective studies and related experimental studies are needed to further validate the conclusions of this study.

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“…Specifically, M1 macrophages produce liver TNF‐α, whereas the efficiency of TNF‐α secretion by M2 macrophages is low. M1 macrophages produce IL‐12 and IL‐1β and promote T cells to produce IFN‐γ 16,17 . In contrast, M2 macrophages mainly produce IL‐10 and IL‐1 receptor antagonists, inhibiting T cell expression of IFN‐γ 18,19 .…”

Section: Introductionmentioning

confidence: 99%

“…M1 macrophages produce IL-12 and IL-1β and promote T cells to produce IFN-γ. 16,17 In contrast, M2 macrophages mainly produce IL-10 and IL-1 receptor antagonists, inhibiting T cell expression of IFN-γ. 18,19 It has been reported that TNF-α and IFN-γ expression in the liver is primarily determined by liver macrophages [20][21][22] ; thus, cytokine-regulating macrophage activation may reduce T-cell-dependent production of liver IFN-γ and TNF-α.…”

Section: Introductionmentioning

confidence: 99%

Interleukin 28A aggravates Con A‐induced acute liver injury by promoting the recruitment of M1 macrophages

Zhang,

Cheng,

Zhang

et al. 2024

The FASEB Journal

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Immune‐mediated acute hepatic injury is characterized by the destruction of a large number of hepatocytes and severe liver function damage. Interleukin‐28A (IL‐28A), a member of the IL‐10 family, is notable for its antiviral properties. However, despite advances in our understanding of IL‐28A, its role in immune‐mediated acute injury remains unclear. The present study investigated the role of IL‐28A in concanavalin A (Con A)‐induced acute immune liver injury. After Con A injection in mice, IL‐28A level significantly increased. IL‐28A deficiency was found to protect mice from acute liver injury, prolong survival time, and reduce serum aspartate aminotransferase and alanine aminotransferase levels. In contrast, recombinant IL‐28A aggravated liver injury in mice. The proportion of activated M1 macrophages was significantly lower in the IL‐28A‐deficiency group than in the wild‐type mouse group. In adoptive transfer experiments, M1 macrophages from WT could exacerbate mice acute liver injury symptoms in the IL‐28A deficiency group. Furthermore, the expression of proinflammatory cytokines, including tumor necrosis factor‐α (TNF‐α), IL‐12, IL‐6, and IL‐1β, by M1 macrophages decreased significantly in the IL‐28A‐deficiency group. Western blotting demonstrated that IL‐28A deficiency could limit M1 macrophage polarization by modulating the nuclear factor (NF)‐κB, mitogen‐activated protein kinase (MAPK), and interferon regulatory factor (IRF) signaling pathways. In summary, IL‐28A deletion plays an important protective role in the Con A‐induced acute liver injury model and IL‐28A deficiency inhibits the activation of M1 macrophages by inhibiting the NF‐κB, MAPK, and IRF signaling pathways. These results provide a potential new target for the treatment of immune‐related hepatic injury.

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N,N-dimethylformamide-induced acute liver damage is driven by the activation of NLRP3 inflammasome in liver macrophages of mice

Cited by 10 publications

References 43 publications

Manganese dioxide nanoparticles provoke inflammatory damage in BV2 microglial cells via increasing reactive oxygen species to activate the p38 MAPK pathway

Manganese dioxide nanoparticles provoke inflammatory damage in BV2 microglial cells via increasing reactive oxygen species to activate the p38 MAPK pathway

The exposure to volatile organic chemicals associates positively with rheumatoid arthritis: a cross-sectional study from the NHANES program

Interleukin 28A aggravates Con A‐induced acute liver injury by promoting the recruitment of M1 macrophages

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