Polystyrene microplastics lead to pyroptosis and apoptosis of ovarian granulosa cells via NLRP3/Caspase-1 signaling pathway in rats

Hou, Junyu; Lei, Zhimin; Cui, Linlu; Hou, Yun; Long, Yang; An, Ru; Wang, Qimeng; Li, Shengda; Zhang, Hongqin; Zhang, Lianshuang

doi:10.1016/j.ecoenv.2021.112012

Cited by 211 publications

(116 citation statements)

References 65 publications

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“…Similar translocations of nanoplastics have been found to originate from the lungs via inhalation (Choi et al 2010 ). Animal models have found microplastic accumulation in mammalian male (Jin et al 2021 ) and female (An et al 2021 ; Hou et al 2021 ) gonadal tissues, possibly affecting fertility and reproductive capacity. Inside the body, in addition to their physical and mechanical interactions, microplastics can also leach chemical into tissues and circulation, including chemicals applied during manufacturing (e.g., bisphenols, phthalates, perfluoridated compounds, brominated flame retardants, UV stabilizers) (Cox et al 2019 ) and for aged plastics, substances absorbed and accumulated from the environment (e.g., organic pesticides, polyaromatic hydrocarbons, heavy metals, and pathogens) (Alimba and Faggio 2019 ; Cox et al 2019 ; Scopetani et al 2018 ; Torres et al 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Polystyrene and Polyethylene Microplastics Decrease Cell Viability and Dysregulate Inflammatory and Oxidative Stress Markers of MDCK and L929 Cells In Vitro

2021

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Microplastics are ubiquitous environmental pollutants that are a growing concern to many ecosystems, as well as human health. Many of the effects of microplastics on mammalian cells and tissues remain unknown. To address this, we treated L929 murine fibroblasts and Madin–Darby canine kidney (MDCK) epithelial cell lines with 1 μg/mL, 10 μg/mL, or 20 μg/mL of polyethylene (PE) or polystyrene (PS) microspheres in vitro for 6 and 24 h and measured the resulting changes in cell viability, metabolism, and transcriptional expression of inflammatory cytokines and antioxidant enzymes. We observed dose-dependent decreases in cell viability corresponding to increases in doses of both PE and PS. We conducted cell metabolism assays and observed dose-dependent increases in metabolism per cell with increasing doses of both PE and PS. Similarly, we also observed increased expression of the superoxide dismutase-3 gene ( SOD3 ), indicating oxidative stress caused by the microplastics treatments. We also observed increased expression of TNFα , but decreased expression of IFNβ , suggesting different mechanisms by which the microplastics regulate inflammatory responses in mammalian cells. Our results contribute new data to the growing understanding of the effects of microplastics on mammalian cells and indicate complex cellular stress responses to microplastics in the environment.

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Section: Introductionmentioning

confidence: 99%

Polystyrene and Polyethylene Microplastics Decrease Cell Viability and Dysregulate Inflammatory and Oxidative Stress Markers of MDCK and L929 Cells In Vitro

2021

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“…Besides, PAE is capable of noticeably rising programmed cell death-related protein (P65, NF-KB, MyD88, and TLR4) within gastric tissue under the cause of ethanol. Besides, when cells undergo oxidative stress under the cause of ethanol, they can induce and activate the release of the inflammation-associated factor NLRP3 inflammasome, activate Caspase-1 and eventually mature the effector pro-inflammatory cytokines ( Hou et al, 2021 ). Our study has showed that PAE administration is capable of lowering the stimulation of the NLRP3/caspase-1 channel triggered by ethanol administration, while impacting inflammation and oxidative stress by regulating pro-inflammatory cytokines (IL-18, TNF-α, IL-6, IL-1β) and oxidative stress factors (MPO and SOD).…”

Section: Discussionmentioning

confidence: 99%

Gastroprotective Effects of Periplaneta americana L. Extract Against Ethanol-Induced Gastric Ulcer in Mice by Suppressing Apoptosis-Related Pathways

Chen

Zhang

et al. 2021

Front. Pharmacol.

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Although Periplaneta americana L. and its modern preparation, Kangfuxin liquid, have been extensively applied for ulcerative diseases in gastrointestinal tract (e.g., gastric ulcer (GU) and ulcerative colitis, the effective components and potential mechanisms) remain unclear. In accordance with the accumulating research evidences, the relieving/exacerbating of GU is noticeably correlated to focal tissue programmed cell death. Herein, gastro-protective effects of the effective Periplaneta americana L. extract (PAE) fraction were assessed in vitro and in vivo, involving in programmed cell death-related signaling channels. To screen the effective PAE fraction exerting gastroprotective effects, several PAE fractions were gained based on a wide range of ethanol solution concentration, and they were assessed on ethanol-induced ulcer mice. Based on HPLC investigation with the use of nucleosides, the chemical composition of screened effective PAE, extracted by 20% ethanol, was analyzed in terms of quality control. Based on CCK-8 assay, the protective effects on GES-1 cells, impaired by ethanol, of PAE were assessed. After 3 days pre-treatment with PAE (200, 400, 800 mg/kg), the gastric lesions were assessed by tissue morphology, and periodic acid-schiff (PAS) staining, as well as hematoxylin and eosin (H&E) based histopathology-related investigation. The levels for inflammation cytokines (IL1-β, TNF-α, IL-18, PGE2, and IL-6), antioxidant indices (SOD and MDA) were examined via ELISA. In the meantime, based on Western Blotting assay, the expression levels of some programmed cell death-related protein targets (NLRP3, caspase-1, NF-κB p65, MyD88, and TLR4) were analyzed. As revealed from the results, PAE is capable of alleviating gastric mucosa impairment, suppressing the inflammatory cytokines, and down-regulating the MyD88/NF-κB channels. Accordingly, 20% ethanol extract of Periplaneta americana L. would contribute its gastroprotective effects, thereby providing the evidence that its anti-GU mechanisms correlated with inhibiting programmed cell death channel.

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“…Studies have shown that pyroptosis is involved in various diseases, particularly neurodegenerative diseases (Voet et al, 2019;Zhao et al, 2019). It is reported that polystyrene microplastics, which continuously pollute the environment, can induce pyroptosis and apoptosis of ovarian granulosa cells via the NLRP3/caspase-1 signaling pathway triggered by oxidative stress (Hou et al, 2021). Moreover, the activation of NLRP3 plays an important role in caspase-1-dependent pyroptosis.…”

Section: Bpa May Induce Pyroptosis By Nlrp3/caspase-1/gsdmd Signaling Pathwaymentioning

confidence: 99%

Involvement of NLRP3/Caspase-1/GSDMD-Dependent Pyroptosis In BPA-Induced Apoptosis of Neuroblastoma Cells

Wang

Huang

et al. 2021

Preprint

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BackgroundBisphenol A (BPA) is an additive in polycarbonate and epoxy resin particles with endocrine disrupting effects. Previously it has been reported that BPA is neurotoxic via induction of cell apoptosis and inflammation, and our recent studies showed that even at nanomolar concentrations BPA accelerated the apoptosis and death of human neuroblastoma cells from both genders, whose mechanisms remain, however, unidentified.ResultsHuman neuroblastoma cell lines developed from male and female subjects, IMR-32 and SK-N-SH, respectively, were exposed to BPA at concentrations ranging from 1 nM to 100 μM, for 24 h, with or without epigallocatechin gallate (EGCG, 4 or 8 μM), Z-YVAD-FMK (1 or 10 μM, caspase-1 inhibitor), and ICI182.780 (100 nM or 3 μM, estrogen receptor inhibitor) as modulators. The results showed that BPA nonlinearly upregulated the levels of IL-18, ASC, GSDMD and NLRP3 mRNAs and that of NLRP3, caspase-1, GSDMD and IL-1β proteins in IMR-32 and SK-N-SH cells. Noticeably, the mRNA levels of caspase-1 and IL-1β were changed differently in the two cell lines: the level of caspase-1 mRNA was enhanced in IMR-32 cells but suppressed in SK-N-SH cells, and that of IL-1β was suppressed in IMR-32 cells but enhanced in SK-N-SH cells. The level of GSDMD expression in situ was along with the increase in the release of IL-1β, IL-18, caspase-1 and lactate dehydrogenase (LDH). Additionally, Z-YVAD-FMK, ICI182.780 and EGCG significantly reversed the changes of the above mRNAs/proteins induced by BPA. BPA significantly reduced the level of the reactive oxygen species and the rate of LDH leakage and apoptosis, while obviously increased the cell viability and the mitochondrial membrane potential. Meanwhile, Z-YVAD-FMK and ICI182.780 abruptly reduced the levels of Bak1, Bax, Bcl-2 and caspase-3 proteins induced by BPA. ConclusionAs mediated by the estrogen receptor, BPA may induce the pyroptosis of neuroblastoma cells through NLRP3/caspase-1/GSDMD signaling pathway, and caspase-1-dependent pyroptosis may be involved in BPA-induced apoptosis, which is alleviated by EGCG, an anti-oxidation agent.

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Polystyrene microplastics lead to pyroptosis and apoptosis of ovarian granulosa cells via NLRP3/Caspase-1 signaling pathway in rats

Cited by 211 publications

References 65 publications

Polystyrene and Polyethylene Microplastics Decrease Cell Viability and Dysregulate Inflammatory and Oxidative Stress Markers of MDCK and L929 Cells In Vitro

Polystyrene and Polyethylene Microplastics Decrease Cell Viability and Dysregulate Inflammatory and Oxidative Stress Markers of MDCK and L929 Cells In Vitro

Gastroprotective Effects of Periplaneta americana L. Extract Against Ethanol-Induced Gastric Ulcer in Mice by Suppressing Apoptosis-Related Pathways

Involvement of NLRP3/Caspase-1/GSDMD-Dependent Pyroptosis In BPA-Induced Apoptosis of Neuroblastoma Cells

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