4.7 Article

The mechanism of acrolein exposure inhibited the release of neutrophil extracellular traps: By reducing respiratory burst and Raf/MEK/ERK pathway and promote cell apoptosis

相关参考文献

注意:仅列出部分参考文献,下载原文获取全部文献信息。
Article Environmental Sciences

Glyphosate-induced autophagy inhibition results in hepatic steatosis via mediating epigenetic reprogramming of PPAR? in roosters

Cai-Yu Lian et al.

Summary: This study investigates the mechanisms of Glyphosate-induced hepatic steatosis using a rooster model and primary chicken embryo hepatocytes. The results show that Glyphosate exposure caused liver injury and disrupted lipid metabolism, leading to lipid accumulation. Transcriptomic analysis reveals the involvement of PPAR alpha and autophagy-related pathways in Glyphosate-induced hepatic lipid metabolism disorders.

ENVIRONMENTAL POLLUTION (2023)

Article Agriculture, Multidisciplinary

Cannabidiol Alleviates Perfluorooctanesulfonic Acid-Induced Cardiomyocyte Apoptosis by Maintaining Mitochondrial Dynamic Balance and Energy Metabolic Homeostasis

Xixi Wang et al.

Summary: It has been found that PFOS causes cardiac toxicity and CBD can attenuate the PFOS-induced heart injury, providing a novel cardioprotective strategy.

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY (2023)

Article Environmental Sciences

Cannabidiol alleviates perfluorooctane sulfonate-induced macrophage extracellular trap mediate inflammation and fibrosis in mice liver

Dongliu Luo et al.

Summary: This study investigates the effects of perfluorooctane sulphonate (PFOS) on liver injury and the potential protective role of cannabidiol (CBD). Results showed that PFOS exposure induces inflammatory infiltration, macrophage extracellular trap (MET) formation, and fibrosis in the liver. In vitro experiments also demonstrated that PFOS can induce inflammation and fibrosis marker gene expression. However, CBD treatment was found to alleviate PFOS-induced liver injury by inhibiting MET release through interaction with PAD4.

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY (2023)

Article Biochemistry & Molecular Biology

Acrolein produced by glioma cells under hypoxia inhibits neutrophil AKT activity and suppresses anti-tumoral activities

Hong-Chieh Tsai et al.

Summary: Acrolein, a reactive aldehyde, is generated during lipid peroxidation in a hypoxic environment and can form bonds with cysteine residues, leading to functional changes in proteins and immune suppression. Neutrophils play a critical role in the immune response, with proinflammatory N1 neutrophils exerting antitumor effects and anti-inflammatory N2 neutrophils supporting tumor growth. Glioma is characterized by hypoxia, immune cell infiltration, and an immunosuppressive microenvironment. Previous studies have shown that neutrophils exhibit an antitumor phenotype in early glioma development but transition to a tumor-supporting role as the tumor progresses. However, the mechanism behind this switch in neutrophil phenotype remains unclear. This study demonstrates that acrolein production in glioma cells inhibits neutrophil activation and induces an anti-inflammatory phenotype by directly interacting with AKT and inhibiting its activity. Moreover, higher levels of acrolein adducts in tumor tissue are associated with poorer prognosis in glioblastoma patients, and high-grade glioma patients exhibit increased serum acrolein levels and impaired neutrophil functions. These findings highlight the importance of acrolein in suppressing neutrophil function and contributing to the switch in neutrophil phenotype in glioma.

FREE RADICAL BIOLOGY AND MEDICINE (2023)

Article Engineering, Environmental

ERK/p38/ROS burst responses to environmentally relevant concentrations of diphenyl phosphate-evoked neutrophil extracellular traps formation: Assessing the role of autophagy

Siwen Li et al.

Summary: The study revealed that diphenyl phosphate (DPHP) could promote the formation of neutrophil extracellular traps (NETs) by inducing reactive oxygen species (ROS) burst and activation of extracellular signal-regulated kinase (ERK) and p38, as well as triggering autophagy. Inhibition of autophagy could alleviate the ROS burst and subsequent NETosis caused by DPHP, while enhancing autophagy could augment these effects. This indicated that ERK/p38 signaling and ROS burst may play a crucial role in DPHP-induced NETs formation, and excessive autophagy suppression could rescue these actions.

JOURNAL OF HAZARDOUS MATERIALS (2022)

Article Engineering, Environmental

Epigenetic regulator BRD4 is involved in cadmium-induced acute kidney injury via contributing to lysosomal dysfunction, autophagy blockade and oxidative stress

Zhong-Gui Gong et al.

Summary: The study demonstrates that BRD4 acts as a transcriptional repressor in mediating lysosomal dysfunction, autophagy blockade, and oxidative stress during Cd exposure, showing its potential as a therapeutic target for Cd-induced AKI.

JOURNAL OF HAZARDOUS MATERIALS (2022)

Article Pharmacology & Pharmacy

Resveratrol protected acrolein-induced ferroptosis and insulin secretion dysfunction via ER-stress- related PERK pathway in MIN6 cells

Xinhao Zhang et al.

Summary: Acrolein, a common food and environmental pollutant, induces ferroptosis in pancreatic beta cells, leading to dysfunction. Endoplasmic reticulum stress plays a critical role in acrolein-induced ferroptosis. Resveratrol can alleviate ER stress and protect pancreatic cells from acrolein-induced damage.

TOXICOLOGY (2022)

Article Pharmacology & Pharmacy

Toxicity mechanism of acrolein on DNA damage and apoptosis in BEAS-2B cells: Insights from cell biology and molecular docking analyses

Dan Liu et al.

Summary: This study reveals that acrolein induces DNA damage and mitochondrial apoptosis in human bronchial epithelial cells, which may be the pivotal factors mediating its cytotoxicity.

TOXICOLOGY (2022)

Article Biochemistry & Molecular Biology

Interaction between iron oxide nanoparticles (Fe3O4 NPs) and human neutrophils: Evidence that Fe3O4 NPs possess some pro-inflammatory activities

Abdelaziz Saafane et al.

Summary: This study investigated the direct effects of Fe3O4 NPs on neutrophils and found that they enhance neutrophil adhesion and phagocytosis, delay neutrophil apoptosis, and induce the production of pro-inflammatory cytokines.

CHEMICO-BIOLOGICAL INTERACTIONS (2022)

Article Engineering, Environmental

Polystyrene nanoparticle exposure supports ROS-NLRP3 axis-dependent DNA-NET to promote liver inflammation

Qianru Chi et al.

Summary: The use of plastics and nanotechnology has brought convenience to our lives, but it also increases the environmental burden and the risk of exposure to nanoparticles. This study reveals that exposure to polystyrene nanoparticles (PSNPs) leads to neutrophil infiltration and neutrophil extracellular trap (NET) formation in the liver. Further research shows that NET formation is associated with the reactive oxygen species (ROS)-NLRP3 axis. Inhibition of ROS and NLRP3 can alleviate PSNP-induced NET formation. Moreover, the use of DNase I-coated PSNPs can disassemble NET, reduce neutrophil infiltration in the liver, inhibit the ROS-NLRP3 axis, and decrease cytokine expression.

JOURNAL OF HAZARDOUS MATERIALS (2022)

Article Engineering, Environmental

ROS-Induced Hepatotoxicity under Cypermethrin: Involvement of the Crosstalk between Nrf2/Keap1 and NF-κB/iκB-α Pathways Regulated by Proteasome

Hongjing Zhao et al.

Summary: The study focused on the toxic effects of Cypermethrin on grass carp, showing hepatotoxicity in terms of pathological changes, oxidative stress, and apoptosis in the liver. RNA-Seq analysis suggested that proteasome and oxidative phosphorylation pathways were compromised under CMN exposure, leading to toxic effects. In vitro studies further confirmed that proteasome pathway inhibition could protect against CMN-induced toxicity by enhancing antioxidative and anti-inflammatory capability.

ENVIRONMENTAL SCIENCE & TECHNOLOGY (2021)

Article Biochemistry & Molecular Biology

Roles of selenoprotein S in reactive oxygen species-dependent neutrophil extracellular trap formation induced by selenium-deficient arteritis

Qianru Chi et al.

Summary: Selenium deficiency induces arteritis by reducing SelS levels and promotes disease progression by regulating neutrophil recruitment and NET formation. The formation of NETs in arteritis is dependent on ROS bursts and the PPAR pathway. Silencing SelS exacerbates arteritis through its effects on NET formation.

REDOX BIOLOGY (2021)

Article Environmental Sciences

The antagonistic effect of Se on the Pb-weakening formation of neutrophil extracellular traps in chicken neutrophils

Kai Yin et al.

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY (2019)

Article Immunology

Entamoeba histolytica Induce Signaling via Raf/MEK/ERK for Neutrophil Extracellular Trap (NET) Formation

Zayda Fonseca et al.

FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY (2018)

Article Medicine, General & Internal

Cigarette smoke condensate attenuates phorbol ester-mediated neutrophil extracellular trap formation

Refilwe Philadelphia Bokaba et al.

AFRICAN HEALTH SCIENCES (2017)

Article Biochemistry & Molecular Biology

Activation versus inhibition of microsomal glutathione S-transferase activity by acrolein. Dependence on the concentration and time of acrolein exposure

Mireille M. J. P. E. Sthijns et al.

CHEMICO-BIOLOGICAL INTERACTIONS (2017)

Article Medicine, Research & Experimental

A role for muscarinic receptors in neutrophil extracellular trap formation and levamisole-induced autoimmunity

Carmelo Carmona-Rivera et al.

JCI INSIGHT (2017)

Article Biochemistry & Molecular Biology

Acrolein activates cell survival and apoptotic death responses involving the endoplasmic reticulum in A549 lung cells

Andre Tanel et al.

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH (2014)

Article Environmental Sciences

Acrolein Induction of Oxidative Stress and Degranulation in Mast Cells

Daniel J. Hochman et al.

ENVIRONMENTAL TOXICOLOGY (2014)

Article Biochemistry & Molecular Biology

Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines

Christine Schauer et al.

NATURE MEDICINE (2014)

Article Biochemistry & Molecular Biology

Lithium Prevents Acrolein-Induced Neurotoxicity in HT22 Mouse Hippocampal Cells

Yingjuan Huang et al.

NEUROCHEMICAL RESEARCH (2014)

Article Biochemistry & Molecular Biology

Activation of the Raf-MEK-ERK pathway is required for neutrophil extracellular trap formation

Abdul Hakkim et al.

NATURE CHEMICAL BIOLOGY (2011)

Article Toxicology

Nonredundant functions of αβ and γδ T cells in acrolein-induced pulmonary pathology

Michael T. Borchers et al.

TOXICOLOGICAL SCIENCES (2008)

Review Public, Environmental & Occupational Health

Acrolein environmental levels and potential for human exposure

O. Faroon et al.

TOXICOLOGY AND INDUSTRIAL HEALTH (2008)

Article Multidisciplinary Sciences

Neutrophil extracellular traps kill bacteria

V Brinkmann et al.

SCIENCE (2004)

Article Biochemistry & Molecular Biology

Acrolein induces axolemmal disruption, oxidative stress, and mitochondrial impairment in spinal cord tissue

H Luo et al.

NEUROCHEMISTRY INTERNATIONAL (2004)

Article Biochemistry & Molecular Biology

Acrolein-induced cell death: a caspase-influenced decision between apoptosis and oncosis/necrosis

JC Kern et al.

CHEMICO-BIOLOGICAL INTERACTIONS (2002)