Acrylamide induces NLRP3 inflammasome activation via oxidative stress- and endoplasmic reticulum stress-mediated MAPK pathway in HepG2 cells

Nan, Bo; Yang, Hong; Yang, Chaoyue; Lu, Li; Yuan, Yuan

doi:10.1016/j.fct.2020.111679

Cited by 36 publications

(14 citation statements)

References 51 publications

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“…It has been reported that cigarette smoke could increase the NLRP3 in ammatory complex and activate NF-κB pathway in THP-1 cells (Mehta and Dhawan 2020). In this study, the distribution of p65 in the nucleus increased and the phosphorylation of IκB increased after COFs treatment, and this result was consistent with the toxicity induce by acrylamide in HepG2 cells (Bo et al 2020). the mechanism of COFs induced in ammatory response of Beas-2B cells may be to activate NF-κB signaling pathway.…”

supporting

confidence: 85%

The toxicity of cooking oil fumes on human bronchial epithelial cells through ROS‐mediated MAPK, NF‐κB signaling pathways and NLRP3 inflammasome

Liu

Miao

et al. 2022

Environmental Toxicology

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Cooking oil fumes (COFs) are main pollutants in kitchen and indoor air, which threaten human health.Exposure to COFs can cause respiratory diseases and impair pulmonary function. To investigate the toxicity of COFs on human bronchial epithelial cells (Beas-2B) and explore the underlying mechanisms, MTT assay was conducted to detect the viability of Beas-2B. Intracellular reactive oxygen species (ROS) levels and nitric oxide (NO) levels were determined with DCFH-DA assay and DAF-FM assay. The expression of genes involved in in ammation were measured with quantitative real-time PCR (qRT-PCR).The phosphorylation and the expression of proteins related to Mitogen-activated protein kinase (MAPK), NF-κB signaling pathways were measured with western blot. Our results revealed that COFs decreased Beas-2B cells viability, increased the ROS levels and NO levels in cells and induced apoptosis in Beas-2B cells. The results of qRT-PCR and western blot showed that the expression of NLRP3, p65, iNOS, IL-1β, and the factors related to oxidative stress and in ammation increased, NF-κB signaling pathway and MAPK signaling pathway were activated. This study provided some useful information to alleviate the toxicity of COFs and revealed the possible mechanism for the damage on respiratory system induced by COFs. et al. 2015;Wang et al. 2018).COFs pollution produced by cooking usually includes ketones, aldehydes, hydrocarbons, fatty acids, alcohols, aromatic compounds, esters, heterocycles, and lactones is a serious health risk in china due to the cooking manners (Ding et al. 2020;Lee and Gany 2013). In China alone, the number of people exposed to COFs in 2018 has reached to 240 million and most of whom were middle-aged women . Women exposed to COFs are at higher risk for chronic bronchitis, for pregnant women, such exposure can also affect the fetus and increase the risks of adverse birth outcomes (Hou et al. 2018;Vavalà et al. 2014;Zhu et al. 2019). Studies have shown that exposure to COFs increased the risk of respiratory diseases, such as airway infection, chronic obstructive pulmonary disease, tuberculosis and

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supporting

confidence: 85%

The toxicity of cooking oil fumes on human bronchial epithelial cells through ROS‐mediated MAPK, NF‐κB signaling pathways and NLRP3 inflammasome

Liu

Miao

et al. 2022

Environmental Toxicology

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“…Finally, food consumed as such, or after cooking processes, as well as water, may also contain internal or accidental components with a stimulating effect on NLRP3 inflammasome. Among these, mycotoxins (zearalenone, patulin, deoxynivalenol), trace metals (arsenic, cadmium), environmental and food contaminants (acrolein, 3-monochloropropane-1,2-diol, glycidol, and its esters), and acrylamide are few examples of NLRP3 activators, endowed with harmful inflammatory effects [ 212 , 213 , 214 , 215 , 216 , 217 , 218 , 219 , 220 ].…”

Section: Food and Nutraceuticals Components Bioavailability And Toxicitymentioning

confidence: 99%

Modulatory Properties of Food and Nutraceutical Components Targeting NLRP3 Inflammasome Activation

et al. 2022

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Inflammasomes are key intracellular multimeric proteins able to initiate the cellular inflammatory signaling pathway. NLRP3 inflammasome represents one of the main protein complexes involved in the development of inflammatory events, and its activity has been largely demonstrated to be connected with inflammatory or autoinflammatory disorders, including diabetes, gouty arthritis, liver fibrosis, Alzheimer’s disease, respiratory syndromes, atherosclerosis, and cancer initiation. In recent years, it has been demonstrated how dietary intake and nutritional status represent important environmental elements that can modulate metabolic inflammation, since food matrices are an important source of several bioactive compounds. In this review, an updated status of knowledge regarding food bioactive compounds as NLRP3 inflammasome modulators is discussed. Several chemical classes, namely polyphenols, organosulfurs, terpenes, fatty acids, proteins, amino acids, saponins, sterols, polysaccharides, carotenoids, vitamins, and probiotics, have been shown to possess NLRP3 inflammasome-modulating activity through in vitro and in vivo assays, mainly demonstrating an anti-NLRP3 inflammasome activity. Plant foods are particularly rich in important bioactive compounds, each of them can have different effects on the pathway of inflammatory response, confirming the importance of the nutritional pattern (food model) as a whole rather than any single nutrient or functional compound.

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“…Our previous study also displayed that AA could induce the toxicity through the oxidant damage in brain of rats (Zhao, Wang, Hu, Chen, & Chan, 2017). Various oxidant‐stress‐related signaling pathways, such as MAPK, NF‐κB, and Nrf2, have been found to play a key role in AA toxicity (Bo, Yilin, Chaoyue, Lu, & Yuan, 2020; Pan et al., 2017), and the chemical and biochemical mechanisms of AA have been extensively studied, accompanied by the performed transcriptome and proteomics profiles in cell and animal models (Chepelev et al., 2018; Zhao et al., 2019). However, the details of AA toxicity were obscure, therefore, it is very important that new means have been found out and used to explore the mechanism of AA toxicity.…”

Section: Introductionmentioning

confidence: 99%

Acrylamide alters the miRNA profiles and miR‐27a‐5p plays the key role in multiple tissues of rats

Zhang

Yang

et al. 2020

Food Frontiers

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Acrylamide (AA) is the potential carcinogen, which can induce multiple toxic effects in laboratory animals and humans. So far, increasing attention have been paid to toxical mechanism and intervention measures of AA, however, these details and methods are still obscure. MicroRNAs (miRNAs) have been demonstrated to be involved in toxical functional mechanisms induced by chemicals in vivo or vitro. To explore novel target and mechanism of AA toxicity, a more detailed miRNA expression profiling study is needed. In this study, we established the short‐term high‐dose model of rats with the treatment of 35 mg/kg·b.w./day AA for 17 days, analyzed the miRNAs expression profiling in AA and control groups, and discovered the altered miRNA profiles in 11 tissues with AA treatment. Interestingly enough, the expression of miR‐27a‐5p were significantly up‐regulated in AA group, especially in bladder and hepar. Furthermore, we found miR‐27a‐5p increased in 11 tissues of long‐term low‐dose AA‐treated rats (3.5 mg/kg·b.w./day for 68 days). Therefore, these results revealed that AA changed miRNAs profiles in multiple tissues of SD rats for the first time and suggested that miR‐27a‐5p could be used as the target biomarker for the detection and interference of AA toxicity.

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Acrylamide induces NLRP3 inflammasome activation via oxidative stress- and endoplasmic reticulum stress-mediated MAPK pathway in HepG2 cells

Cited by 36 publications

References 51 publications

The toxicity of cooking oil fumes on human bronchial epithelial cells through ROS‐mediated MAPK, NF‐κB signaling pathways and NLRP3 inflammasome

The toxicity of cooking oil fumes on human bronchial epithelial cells through ROS‐mediated MAPK, NF‐κB signaling pathways and NLRP3 inflammasome

Modulatory Properties of Food and Nutraceutical Components Targeting NLRP3 Inflammasome Activation

Acrylamide alters the miRNA profiles and miR‐27a‐5p plays the key role in multiple tissues of rats

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