Human & experimental toxicology最新文献

{"title":"Expression of concern.","authors":"","doi":"10.1177/09603271241310364","DOIUrl":"https://doi.org/10.1177/09603271241310364","url":null,"abstract":"","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271241310364"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the utility of zinc finger protein-related genes in predicting hepatocellular carcinoma prognosis, immune responses, and drug efficacy.","authors":"Pengtao Zhai, Mei Li, Yuan Cheng","doi":"10.1177/09603271251340277","DOIUrl":"https://doi.org/10.1177/09603271251340277","url":null,"abstract":"<p><p>BackgroundHepatocellular carcinoma (LIHC), a prevalent liver cancer with a grim prognosis due to high recurrence rates, is under scrutiny for its association with zinc finger proteins (ZNFs) in tumorigenesis. This study aims to create a prognostic model for LIHC incorporating ZNF-related genes.MethodsBy analyzing TCGA data, we identified differentially expressed genes (DEGs) between normal and LIHC samples, focusing on ZNF-related genes through univariate Cox and LASSO Cox regression. A multivariate Cox regression model was built, categorizing LIHC patients into high- and low-ZNFRS groups based on ZNF-related risk scores. Model performance was evaluated using ROC curves, with a nomogram integrating clinical data and ZNFRS. Immune microenvironment, enrichment analysis, mutations, and drug responses in LIHC were also explored.ResultsA prognostic model utilizing 10 ZNF-related genes accurately predicted LIHC survival. The low-risk group exhibited enhanced immune cell infiltration, contrasting with cell cycle and DNA replication enrichment in the high-risk group, which also displayed increased mutation rates. Promising drug candidates like SNS-314 and Decitabine warrant further investigation in LIHC treatment.ConclusionThis study introduces impactful prognostic markers for LIHC management, emphasizing the significance of ZNFs in predicting patient outcomes and guiding treatment strategies.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251340277"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physalin A induces apoptosis through conjugating with Fas-FADD cell death receptor in human oral squamous carcinoma cells and suppresses HSC-3 cell xenograft tumors in NOD/SCID mice.","authors":"Fu-Shin Chueh, Sheng-Yao Hsu, Kuang-Chi Lai, Yi-Chung Liu, Ping-Chiang Lyu, Yueh-Hsiung Kuo, Yi-Ping Huang, Wen-Tsong Hsieh","doi":"10.1177/09603271251335220","DOIUrl":"https://doi.org/10.1177/09603271251335220","url":null,"abstract":"<p><p>IntroductionOral carcinoma cancer exhibits high global incidence and mortality. Physalin A (PA) was reported to induce programmed cell death in cancer cells. No study has yet investigated the influence of PA in oral squamous cell carcinoma. Herein, this study aims to explore PA-induced anti-cancer effects in human oral carcinoma.MethodsThis study used DNA gel electrophoresis and Annexin V/PI staining to detect DNA fragmentation and cell apoptosis. Western blotting and immunofluorescence analyzed protein expression. Flow cytometry measured Ca²⁺ release and mitochondrial membrane potential (∆Ψm). Moreover, molecular docking models predicted the molecular binding affinity.ResultsDNA gel electrophoresis and annexin V/PI staining confirmed PA-induced DNA fragmentation and apoptosis. Flow cytometry showed PA increased Ca²⁺ release and reduced ∆Ψm levels. PA activated cleaved caspase-3, -8, and -9, upregulated Bax and Bid, and downregulated Bcl-2. PA dose-dependently increased Fas (CD95/APO-1), apoptosis-inducing factor (AIF), and cytochrome c release in western blotting analysis. Confocal microscopy confirmed increased Bax, AIF, cleaved caspase-3, and Fas, with decreased Bcl-2. Molecular docking showed strong PA binding via hydrophobic interactions with the Fas-associated death domain (FADD). Compared with cisplatin, PA inhibited HSC-3 cell xenograft tumor growth in NOD/SCID mice.DiscussionWe reveal that PA binds to the Fas-FADD complex, inducing caspase-8 activation and triggering extrinsic and intrinsic mitochondria-dependent apoptosis in HSC-3 cells. It also suppresses HSC-3 cell xenograft tumors in NOD/SCID mice. These findings suggest PA as a potential anti-oral cancer agent in the future.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251335220"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing breast cancer treatment: Evaluating the efficacy of hyaluronic acid-coated tamoxifen-loaded solid lipid nanoparticles on MCF7 cells.","authors":"Niloufar Ghayoumipour, Hossein Ghafouri","doi":"10.1177/09603271251322531","DOIUrl":"10.1177/09603271251322531","url":null,"abstract":"<p><strong>Introduction: </strong>Tamoxifen (TMX) shows promise in treating breast cancer, but it faces challenges such as poor solubility, instability, and incomplete release when targeting tumors. Additionally, TMX therapy's toxicity is a critical issue in breast cancer treatment. This study aimed to assess the impact of hyaluronic acid (HA)-coated TMX-loaded solid lipid nanoparticles (HA-TMX-SLNs) on MCF7 breast cancer cells.</p><p><strong>Methods: </strong>Solid lipid nanoparticles (SLNs) were prepared using hot homogenization. The HA-TMX-SLNs and TMX-SLNs were characterized and evaluated through transmission electron microscopy (TEM). Cytotoxicity was assessed using the MTT assay, and Western blot analysis was utilized to identify key factors in the cell cycle and apoptosis.</p><p><strong>Results: </strong>The nanoparticles (HA-TMX-SLNs) demonstrated approximately 55% loading efficiency after 100 h. HA-TMX-SLNs exhibited lower cytotoxicity in MCF7 cells compared to other treatments. Significant decreases in expression levels of cyclin-dependent kinase (CDK) 4, Cyclin D1, CDK2, and Bcl2 were observed after treatment with HA-TMX-SLNs, along with an increase in cleaved/procaspase-7.</p><p><strong>Discussion: </strong>The in vitro release study showed that HA-coated SLNs consistently released the drug into the media under controlled conditions. Furthermore, HA-TMX-SLNs exhibited cytotoxic effects, increasing apoptosis and inhibiting cancer cell proliferation. These findings suggest that HA-TMX-SLNs effectively deliver TMX to breast cancer cells.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251322531"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143461174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of SIRT3/AMPK/mTOR-mediated autophagy promotes quercetin-induced ferroptosis in oral squamous cell carcinoma.","authors":"Jin Wang, Jia-Hui Yang, Di Xiong, Ling Chen","doi":"10.1177/09603271251323753","DOIUrl":"10.1177/09603271251323753","url":null,"abstract":"<p><strong>Introduction: </strong>Quercetin has been reported to inhibit the growth of oral squamous cell carcinoma (OSCC), but the mechanism remains unclear. Therefore, our study aimed to investigate the involvement of sirtuin 3 (SIRT3) and the autophagy-dependent form of cell death, ferroptosis, in the pathogenesis of OSCC, and observe the impacts of quercetin on ferroptosis and SIRT3/AMPK/mTOR-mediated autophagy.</p><p><strong>Methods: </strong>SIRT3 knock out or overexpressing SCC15 cell line was generated, treated with indicated drugs, and malondialdehyde (MDA) and ROS levels were measured. Roles of SIRT3 in regulating autophagy-mediated ferroptosis were assessed by immunoprecipitation and Western blotting.</p><p><strong>Results: </strong>SIRT3 overexpression increased levels of MDA and ROS, reducing cell viability, and SIRT3 knockout produced the opposing effect. SIRT3 overexpression upregulated ATG16L1 expression and the conversion of LC3-Ⅰ to LC3-Ⅱ, triggering autophagy. Suppression of autophagy by ATG16L1 knockout impaired SIRT3-triggered ferroptosis. Use of an AMPK inhibitor antagonized the induction of ferroptosis by SIRT3 in SCC15 cells, indicating the involvement of the AMPK/mTOR pathway. Additionally, quercetin significantly increased the levels of SIRT3, p-AMPK, ATG16L1, and the ratio of LC3-Ⅱ/Ⅰ, but reduced cell viability and p-mTOR in SCC15 cells. Autophagy and AMPK inhibitors, or SIRT3 deletion significantly antagonized the impacts of quercetin on the autophagy-mediated ferroptosis in cancer cells.</p><p><strong>Discussion: </strong>SIRT3 overexpression activated the AMPK/mTOR pathway and triggered ATG16L1-mediated autophagy, promoting ferroptosis in SCC15 cells, and we proposed that quercetin may be a promising therapeutic drug for OSCC.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251323753"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143517643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into therapeutic potential and practical applications of natural toxins from poisonous mushrooms.","authors":"Tharuka Wijesekara, Baojun Xu","doi":"10.1177/09603271251323134","DOIUrl":"10.1177/09603271251323134","url":null,"abstract":"<p><p>IntroductionMushrooms, belonging to the phyla Ascomycota and Basidiomycota, comprise approximately 14,000 known species, among which a small fraction are toxic. While toxic mushrooms are primarily associated with adverse health effects, recent research highlights their potential as sources of bioactive compounds with promising therapeutic applications.MethodsA systematic review was conducted using four major electronic databases: Web of Science, Google Scholar, PubMed, and ScienceDirect. The literature search, completed on July 1, 2024, utilized keywords including \"Poisonous mushrooms,\" \"Mushroom toxins,\" \"Mycotoxins,\" \"Beta-glucans,\" \"Psilocybin,\" and \"Therapeutic applications.\" Articles were selected based on specific inclusion criteria, focusing on studies investigating the biochemical, toxicological, and pharmacological properties of toxic mushroom compounds. Studies unrelated to mushrooms, non-peer-reviewed sources, or those with outdated or incomplete data were excluded.ResultsThis review examines key toxic mushroom compounds such as amanitins, phallotoxins, ibotenic acid, muscimol, orellanine, and gyromitrin, emphasizing their biosynthesis, structural features, and health effects. Despite their toxicity, compounds like beta-glucans, polysaccharides, lectins, and psilocybin exhibit immune-modulating, anticancer, and neuroprotective properties. These bioactive compounds have shown promise in targeting cancer stem cells and enhancing neurotransmitter activity, positioning them as potential therapeutic agents.DiscussionUnderstanding the therapeutic potential of toxic mushroom-derived bioactive compounds bridges toxicology and pharmacology, offering novel avenues for drug discovery. Comparative analysis with existing treatments highlights their unique advantages in modern medicine.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251323134"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cigarette smoking extract induces mitochondrial dysfunction and apoptosis in HUVECs via the Sirt1-SHH axis.","authors":"Weiming Wang, Gang Yuan, Guang Li, Tingting Zhao, Yue Chen, Youhua Xu","doi":"10.1177/09603271251332251","DOIUrl":"10.1177/09603271251332251","url":null,"abstract":"<p><p>IntroductionCigarette smoking extract (CSE) can cause endothelial cell (EC) dysfunction, and then promote the occurrence and development of atherosclerosis. However, the molecular mechanisms underlying CSE-induced EC dysfunction are unknown. Sirt1, as a deacetylase, is involved in various biological processes of ECs. Therefore, this study investigated whether CSE induces apoptosis and mitochondrial dysfunction in human umbilical vein endothelial cells (HUVECs) via Sirt1-dependent mechanisms.MethodsHUVEC activity was assessed using MTT and crystal violet staining following treatment with different concentrations of CSE. Lentiviral transfection technology was used to generate HUVECs overexpressing Sirt1. Apoptosis was detected by Tunnel staining. MitoTracker™ Deep Red FM and JC-1 were used to assess mitochondrial structure and membrane potential. ELISA was used to detect the expression of superoxide dismutase (SOD) and malondialdehyde (MDA). qPCR was used to determine mRNA expression. Atherosclerosis was evaluated by oil red O staining in ApoE-KO mice after cigarette smoke exposure.ResultsCSE decreased Sirt1 and sonic hedgehog (SHH) expression, leading to mitochondrial dysfunction and apoptosis in HUVECs. Overexpressing Sirt1 or activating the SHH signaling pathway attenuated CSE-induced apoptosis and mitochondrial dysfunction. However, inhibiting the SHH signaling axis attenuated the protective effect of Sirt1 overexpression on CSE-induced apoptosis and mitochondrial dysfunction. In vivo studies also showed that cigarette smoke exacerbated atherosclerosis in ApoE-KO mice, downregulating Sirt1, SHH, and Gli1 expression in the aorta. Additionally, cigarette smoke increased Bax expression and decreased Bcl-2 expression in ApoE-KO mice aortas.DiscussionsSmoking can affect all stages of the atherosclerosis process, and the specific mechanism remains unclear. This study confirms that CSE can induce mitochondrial dysfunction and apoptosis of HUVECs by reducing Sirt1 expression and inhibiting SHH signaling activation. These findings provide new insights into the prevention and treatment of smoking-induced atherosclerosis.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251332251"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of detergent component sodium dodecyl sulfate on growth hormone secretion in GH3 cells: Implications for pediatric exposure and accidental ingestion.","authors":"Hua Tang, Lanlan Li","doi":"10.1177/09603271251332255","DOIUrl":"10.1177/09603271251332255","url":null,"abstract":"<p><p>IntroductionSodium dodecyl sulfate (SDS), a widely used surfactant in detergents, has raised concerns due to its potential health risks, particularly in children. This study evaluates the impact of SDS exposure on GH secretion in GH3 cells, focusing on oxidative stress as a key mechanism.MethodsGH3 cells were treated with varying concentrations of SDS (0.001-10 mM) for 24 or 48 h. Cell viability was assessed using the MTT assay, while GH secretion was quantified via ELISA. Oxidative stress levels were evaluated through ROS fluorescence assays, and gene expression of Nrf2, IL-6, TNF-α, and caspase-3 was analyzed using qPCR. Additionally, the antioxidant N-acetylcysteine (NAC) was used to determine its protective effects against SDS-induced oxidative stress.ResultsSDS exposure led to a dose-dependent decrease in GH secretion and cell viability, with oxidative stress identified as a primary driver. Nrf2 exhibited a biphasic response, showing transient upregulation at low doses but suppression at higher concentrations, exacerbating oxidative damage. NAC treatment reduced ROS levels and partially restored GH secretion, confirming the role of oxidative stress in SDS-induced toxicity.DiscussionThese findings suggest that SDS exposure may disrupt endocrine function, warranting further risk assessment of its safety in consumer products. Given SDS's prevalence in household products, future research should focus on the long-term effects of SDS exposure to children and potential therapeutic interventions to mitigate oxidative damage.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251332255"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside Re suppresses high glucose-induced apoptosis of placental trophoblasts through endoplasmic reticulum stress-related CHOP/GADD153.","authors":"Guihong Zeng, Weiyang Zou, Changdi Liu, Yulan Chen, Tingmei Wen","doi":"10.1177/09603271241307835","DOIUrl":"10.1177/09603271241307835","url":null,"abstract":"<p><p><b>Background:</b> Gestational diabetes mellitus (GDM) is a metabolic disorder that arises during pregnancy and heightens the risk of placental dysplasia. Ginsenoside Re (Re) may stabilize insulin and glucagon to regulate glucose levels, which may improve diabetes-associated diseases. <b>Purpose:</b> This study aims to investigate the mechanism of Re in high glucose (HG)-induced apoptosis of trophoblasts through endoplasmic reticulum stress (ERS)-related protein CHOP/GADD153. <b>Research Design:</b> Human trophoblast cells HTR-8/SVneo were treated with HG to simulate the HG environment <i>in vitro</i>, while normal glucose (NG) was used as the control. <b>Study Sample:</b> NG (5 mM) or HG (25 mM)-cultured HTR-8/SVneo cells were treated with 10, 20 or 40 μM Re. HG-cultured cells were treated with 5 mM ERS inducer 2-Deoxy-D-glucose (2-DG) and transfected with oe- CHO. <b>Data Collection and/or Analysis:</b> Cell viability and apoptosis were detected by CCK-8 and flow cytometry; LDH release, superoxide dismutase (SOD), malonaldehyde (MDA) and glutathione (GSH) levels were detected using kits; the apoptosisrelated proteins and ERS-related proteins were assessed by western blot. <b>Results:</b> Re (10, 20 or 40 μM) had no significant effect on NG-treated HTR-8/SVneo cell viability. Re (20 or 40 μM) could enhance the viability of HG-treated trophoblasts. Re (40 μM) inhibited apoptosis of HGtreated trophoblasts, ERS and alleviated oxidative stress evidenced by suppressed phosphorylation of PERK, IRE1α, reduced protein expression of ATF6, CHOP/GADD153, and inhibited MDA accumulation, GSH and SOD loss. ERS activation or CHOP/GADD153 overexpression reversed Re's inhibition on HG-induced apoptosis of trophoblasts. <b>Conclusions:</b> Re repressed HG-induced placental trophoblast apoptosis by mediating ERS-related protein CHOP/GADD153.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271241307835"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142967656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Down-regulation of E2F1 attenuates UVB-induced human lens epithelial cell oxidative stress and pyroptosis through inhibiting NLRP3.","authors":"Fang Wang, Fan Yang, Guiqi Yang, Qi Zhou, Hongbin Lv","doi":"10.1177/09603271241309258","DOIUrl":"https://doi.org/10.1177/09603271241309258","url":null,"abstract":"<p><strong>Background: </strong>It is well-known that ultraviolet B (UVB) causes cataracts by inducing pyroptosis and the production of reactive oxygen species (ROS) in human lens epithelial cells (HLECs). The transcription factor E2F1 (E2F1) serves as a positive regulator of disrupted pathways involved in histone modification and cell cycle regulation. However, its function in UVB-treated HLECs remains unknown.<b>Purpose:</b> This study aims to investigate the function of E2F1 in UVB-treated HLECs, with a particular focus on its interaction with NLRP3 and its impact on oxidative stress and pyroptosis. <b>Research Design:</b> HLECs were irradiated with UVB, and cell damage was assessed using CCK-8, ROS, and pyroptosis detection. The interaction between E2F1 and NLRP3 was confirmed using Chromatin immunoprecipitation (ChIP)-qPCR and dual-luciferase reporter assays.<b>Study Sample:</b> The study was conducted using UVB-treated HLECs.</p><p><strong>Data collection and/or analysis: </strong>Collected data were statistically analyzed using one-way analysis of variance (ANOVA).</p><p><strong>Results: </strong>Our results show that HLECs were much more susceptible to oxidative stress, pyroptosis, and E2F1 in response to UVB-irradiation, but that E2F1 down-regulation effectively counteracted these effects. E2F1 was then suggested as a potential NLRP3 transcription factor by bioinformatics studies. At the same time, luciferase and CHIP assays showed that E2F1 could bind to the NLRP3 promoter and enhance NLRP3 transcription. In addition, the protective effects of si-E2F1 against oxidative stress and pyroptosis in HLECs are counteracted by overexpressing NLRP3.</p><p><strong>Conclusions: </strong>All of the above provided the possibility to demonstrate that E2F1 plays a crucial role in regulating oxidative stress and pyroptosis in UVB-induced HLECs through inhibiting NLRP3, and it promotes oxidative stress-induced pyroptosis by suppressing NLRP3 expression.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271241309258"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142934227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}