The role of PSMB5 in sodium arsenite–induced oxidative stress in L-02 cells

Lv, Ying; Hu, Qian; Shi, Mingyang; Wang, Wen; Zheng, Yuancui; Yang, Zhong; Peng, Liuyu; Bi, Dingnian; Zhang, Aihua; Hu, Yong

doi:10.1007/s12192-020-01104-1

Cited by 10 publications

(5 citation statements)

References 28 publications

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“…The overexpression of PSMB5 in human lens epithelial cells has been shown to improve the ability of the cells to tolerate oxidative stress and to increase cell viability, according to research [13]. The expression of PSMB5 was considerably reduced in L02 cells that had been damaged by oxidative stress, whereas Nrf2 activation can boost PSMB5 expression [14]. Additionally, PSMB5 has the ability to protect pluripotent human bone marrow stromal cells from oxidative damage [15].…”

Section: Introductionmentioning

confidence: 99%

PSMB5 Alleviates Ulcerative Colitis by Inhibiting ROS-Dependent NLRP3 Inflammasome-Mediated Pyroptosis

Liu

Hao

et al. 2022

Disease Markers

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Ulcerative colitis (UC) is a chronic inflammatory disease. Intestinal mucosal injury is a significant factor in UC. Pyroptosis is a kind of programmed cell death induced by inflammatory caspases. Proteasome 20S subunit beta 5 (PSMB5) promotes cell viability. The purpose of this study was to determine the impact of PSMB5 on intestinal mucosal injury and to elucidate the underlying processes in dextran sulfate sodium- (DSS-) induced UC mice. Kunming (KM) mice received 3% DSS for 5 days to induce UC. We collected clinical symptoms, body weight, colon length, and histological changes. MDA (malondialdehyde) and SOD (superoxide dismutase) levels were determined using an ELISA assay. RT-PCR was used to assess the expression of IL-1β and IL-18. PSMB5 demonstrated a significant effect against UC by increasing body weight and colon length and decreasing DAI (disease activity index), colon macroscopic damage index (CMDI), histological injury scores, and reactive oxygen species (ROS), MDA, and SOD levels, thereby alleviating histopathological changes and inhibiting oxidative stress. HIEC-6 cells were exposed to lipopolysaccharide (LPS) condition with or without PSMB5, along with caspase-1 inhibitor (Z-VAD-FMK), NLRP3 inhibitor (MCC950), and ROS scavenger N-acetylcysteine (NAC). The viability of the cells, the release of lactate dehydrogenase (LDH), and intracellular ROS generation were determined using assay kits. Western blot analysis was used to determine the levels of NLRP3, ASC, cleaved caspase-1 (p20), pro-IL-1β, IL-1β, pro-IL-18, and IL-18. PSMB5 overexpression enhanced the inflammatory damage in LPS-treated HIEC-6 cells by activating the NLRP3 inflammasome and mediating pyroptosis, as demonstrated by increased LDH release and lower cell viability, as well as increased expression of NLRP3, ASC, cleaved caspase-1 (p20), IL-1, and IL-18. Meanwhile, NAC protected HIEC-6 cells from LPS-induced damage by reversing the activation of the NLRP3 inflammasome-mediated pyroptosis. In conclusion, PSMB5 may lower HIEC-6 cell susceptibility to LPS and ameliorate UC-induced HIEC-6 cell damage by decreasing ROS generation and hence inhibiting NLRP3-mediated pyroptosis.

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Section: Introductionmentioning

confidence: 99%

PSMB5 Alleviates Ulcerative Colitis by Inhibiting ROS-Dependent NLRP3 Inflammasome-Mediated Pyroptosis

Liu

Hao

et al. 2022

Disease Markers

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“…1 A). Thus, we tested a mixture of oleic acid and palmitic acid, which are often used to induce steatosis in vitro (Gómez-Lechón et al 2007 ; Sharma et al 2011 ; Graffmann et al 2016 ; Michaut et al 2016 ); rotenone, a selective complex I inhibitor (Siddiqui et al 2013 ) and carbonylcyanide-p-trifluoromethoxyphenylhydrazone (FCCP), a weak acid that selectively increases proton permeability in lipid membranes (Benz and McLaughlin 1983 ; Sakamuru et al 2016 ), were therefore used as positive controls for inducing mitochondrial dysfunction via a decrease in mitochondrial membrane potential; amiodarone and arsenite, which induce oxidative stress (Anthérieu et al 2011 ; Tolosa et al 2016 ; Zhao et al 2019 ; Lv et al 2020 ); menadione, which induces DNA damage and cell death (Loor et al 2010 ); and caffeine as negative control (Persson et al 2013 ; Saito et al 2016 ) (Fig. 2 ).…”

Section: Resultsmentioning

confidence: 99%

In vitro to in vivo extrapolation and high-content imaging for simultaneous characterization of chemically induced liver steatosis and markers of hepatotoxicity

et al. 2023

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Chemically induced steatosis is characterized by lipid accumulation associated with mitochondrial dysfunction, oxidative stress and nucleus distortion. New approach methods integrating in vitro and in silico models are needed to identify chemicals that may induce these cellular events as potential risk factors for steatosis and associated hepatotoxicity. In this study we used high-content imaging for the simultaneous quantification of four cellular markers as sentinels for hepatotoxicity and steatosis in chemically exposed human liver cells in vitro. Furthermore, we evaluated the results with a computational model for the extrapolation of human oral equivalent doses (OED). First, we tested 16 reference chemicals with known capacities to induce cellular alterations in nuclear morphology, lipid accumulation, mitochondrial membrane potential and oxidative stress. Then, using physiologically based pharmacokinetic modeling and reverse dosimetry, OEDs were extrapolated from data of any stimulated individual sentinel response. The extrapolated OEDs were confirmed to be within biologically relevant exposure ranges for the reference chemicals. Next, we tested 14 chemicals found in food, selected from thousands of putative chemicals on the basis of structure-based prediction for nuclear receptor activation. Amongst these, orotic acid had an extrapolated OED overlapping with realistic exposure ranges. Thus, we were able to characterize known steatosis-inducing chemicals as well as data-scarce food-related chemicals, amongst which we confirmed orotic acid to induce hepatotoxicity. This strategy addresses needs of next generation risk assessment and can be used as a first chemical prioritization hazard screening step in a tiered approach to identify chemical risk factors for steatosis and hepatotoxicity-associated events.

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“…Environmental exposure to arsenic is undoubtedly now a major global public health problem, as well as a serious social and medical problem (Chen et al, 2012;Wang et al, 2020a). Sodium arsenite (NaAsO 2 ) is the most toxic substance of different arsenic compounds in our living environment (Duan et al, 2020;Lv et al, 2020). Accumulation of arsenic in the human body can lead to organ damage and tissue canceration.…”

Section: Introductionmentioning

confidence: 99%

“…Accumulation of arsenic in the human body can lead to organ damage and tissue canceration. In particular, the liver is one of the target organs of arsenic in humans (Dash et al, 2018;Lv et al, 2020). The cellular and molecular biological experiment has shown that arsenic increases the production of reactive oxygen species (ROS) by inhibiting the activity of antioxidant enzymes.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Dictyophora Polysaccharides on Sodium Arsenite-Induced Hepatotoxicity: A Proteomics Study

Shen

Huang

et al. 2021

Front. Pharmacol.

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The purpose of this study is to understand the mechanism of sodium arsenite (NaAsO2)-induced apoptosis of L-02 human hepatic cells, and how Dictyophora polysaccharide (DIP) protects L-02 cells from arsenic-induced apoptosis. The results revealed that DIP pretreatment inhibited NaAsO2 induced L-02 cells apoptosis by increasing anti-apoptotic Bcl-2 expression and decreasing pro-apoptotic Bax expression. Proteomic analysis showed that arsenic treatment disrupted the expression of metabolism and apoptosis associated proteins, including ribosomal proteins (RPs). After pretreatment with DIP, the expression levels of these proteins were reversed or restored. For the first time, it was observed that the significant decrease of cytoplasmic RPs and the increase of mitochondrial RPs were related to human normal cell apoptosis induced by arsenic. This is also the first report that the protective effect of DIP on cells was related to RPs. The results highlight the relationship between RPs and apoptosis, as well as the relationship between RPs and DIP attenuating arsenic-induced apoptosis.

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The role of PSMB5 in sodium arsenite–induced oxidative stress in L-02 cells

Cited by 10 publications

References 28 publications

PSMB5 Alleviates Ulcerative Colitis by Inhibiting ROS-Dependent NLRP3 Inflammasome-Mediated Pyroptosis

PSMB5 Alleviates Ulcerative Colitis by Inhibiting ROS-Dependent NLRP3 Inflammasome-Mediated Pyroptosis

In vitro to in vivo extrapolation and high-content imaging for simultaneous characterization of chemically induced liver steatosis and markers of hepatotoxicity

Protective Effect of Dictyophora Polysaccharides on Sodium Arsenite-Induced Hepatotoxicity: A Proteomics Study

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