HUMAN & EXPERIMENTAL TOXICOLOGY人类与实验毒理学
HUMAN & EXPERIMENTAL TOXICOLOGY(英文缩写 HUM EXP TOXICOL),ISSN 0960-3271,eISSN 1477-0903,中文译名:人类与实验毒理学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.247 | Q3 |
| 2022 | 2.800 | Q3 |
| 2023 | 2.700 | Q3 |
| 2024 | 3.200 | Q2 |
| 2025 | 3.500 | Q2 |
HUMAN & EXPERIMENTAL TOXICOLOGY 最新收录文献
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1. Establishment of a rat model of bronchopulmonary dysplasia complicated with pulmonary hypertension and its potential applications.
PMID:日期:2026-01-27ObjectiveBronchopulmonary dysplasia (BPD), a common chronic lung disease in premature infants, is frequently complicated by pulmonary hypertension (PH), a dangerous condition characterized by elevated pulmonary vascular pressure. At present, the most classic and commonly used animal model for BPD involves exposure to high oxygen concentrations, but existing studies based on this model have seldom addressed whether it recapitulates the pathological features of PH.MethodsIn the present study, we established a rat model of BPD complicated with PH (BPD-PH). Histological hematoxylin and eosin (H&E) staining, enzyme-linked immunosorbent assay (ELISA), flowcytometry, reverse transcription-quantitative PCR (RT-qPCR), wound healing assay, transwell migration and invasion assays, transcriptome RNA-sequencing and GO analysis were performed to evaluate this BPD-PH model.ResultsOur study demonstrated that rats with BPD-PH exhibited characteristic alveolar simplification and features of pulmonary hypertension, including increased mRVP, RV/LV + S and RV/WT. BPD-PH rats had enhanced inflammatory response and increased accumulation of immune cells in lung. Moreover, differentially expressed genes in the BPD-PH rat model were depicted and we found Leucine-rich alpha-2-glycoprotein 1 () was significantly upregulated by 19.32 fold ( < 0.001). LRG1 affected migration, invasion and transforming growth factor-β (TGF-β) signaling activation in primary alveolar epithelial cells and pulmonary endothelial cells. Finally, our BPD-PH model was used for the evaluation of two commonly used drugs for BPD and PH, Dexamethasone and Sildenafil. These two drugs were effective in alleviating lung injury, inflammatory response and hypoxia-induced PH in the rat model of BPD-PH.ConclusionOur data indicate that we established a novel BPD-PH model in rats, and it provided a new choice for the future research for BPD complicated with PH.
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2. {"_":"Pulmonary iron oxide (FeO) nanoparticle-biomolecule interactions modified during aging and metabolic syndrome disease progression.","sub":["3","4"]}
PMID:日期:2026-01-19IntroductionAging and metabolic disease enhance inhaled particulate toxicity. Nanoparticles (NPs) are rapidly coated with biomolecules forming a biocorona (BC), upon entering the body and may contribute to the susceptibility. Aging and metabolic syndrome (MetS) are progressive conditions resulting in biomolecule alterations over time potentially influencing susceptibility. We hypothesize NP-biomolecule interactions are altered during aging and throughout MetS progression.MethodsC57BL/6J mice at 6 weeks of age were fed a healthy diet or a high-fat western diet. BALF was collected after 2, 4, 8, 12, 16, 20 or 24 weeks on diets. NP-biomolecules interactions were compared between healthy and MetS to determine age- and disease progression-related BC variations (proteins and lipids).ResultsUnique BCs were determined to form at each time point indicative of aging for the healthy and aging and disease progression for the MetS. Comparisons between healthy and MetS BCs at each time demonstrated distinct biomolecule interactions attributable to disease. Comparisons determined both unique protein and lipid content as well as quantitative differences. Proteins such as apolipoprotein A-IV, complement C3 and lipids such as PE (37:5), PE (O-38:5), PE (P-38:4), PC(40:7), PC(39:0), and PC(O-40:0) were identified on the MetS BC suggesting disease progression modifications. Proteins such as pulmonary surfactant protein A, fibrinogen alpha-chain and lipids such as CE (19:0)-NH4, DG (36:7), and DG (35:0)_C18:0 were increasingly present in the healthy BC over time, suggesting age-related interactions.DiscussionOverall, unique BCs were identified demonstrating the impact of age and disease progression on BC formation which will aid in understanding initial pulmonary NP-biomolecular interactions potentially contributing to susceptibility.
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3. Inhibition of store-operated calcium entry mitigates lipopolysaccharide-induced hepatotoxicity via modulating inflammatory and oxidative stress responses.
PMID:日期:2026-01-08IntroductionHepatotoxicity can arise secondary to several medical conditions, including inflammation, sepsis, and therapy. Lipopolysaccharide (LPS) can activate diverse inflammatory pathways and has been implicated in hepatotoxicity. The store-operated calcium entry (SOCE), a key process for maintaining cellular calcium homeostasis, was shown to modulate inflammatory signaling. Reactive oxygen species, which serve a significant role in maintaining cellular function and homeostasis, are often elevated during inflammation, contributing to tissue injury. Therefore, we hypothesized that blocking the SOCE pathway would inhibit LPS-induced hepatotoxicity by suppressing inflammation and oxidative stress.MethodsTo test this, female BALB/c mice were randomly divided into the following experimental groups: control, LPS, LPS + SOCE inhibitor 2-aminoethoxy diphenyl borate (2APB), and 2APB alone. After 24 h of treatment, serum and liver samples were collected from the mice for histopathological, biochemical, and molecular analyses.ResultsInhibition of SOCE led to a decrease in the elevated liver function enzymes (ALT and AST) and protected the liver parenchymal cells as observed by histopathological assessment. Furthermore, blockade of SOCE significantly suppressed the level of , , and genes in the liver tissues of mice treated with LPS. The expression of antioxidant genes ( and ) was also significantly reduced by LPS treatment, while SOCE inhibition only restored the expression. Additionally, treatment with 2APB attenuated LPS-induced oxidative stress in the liver of mice.ConclusionCollectively, our work demonstrated the critical involvement of SOCE in regulating inflammation and oxidative stress associated with LPS treatment, thereby reducing hepatotoxicity.
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4. Stevioside inhibits colorectal cancer progression by regulating macrophage polarization.
PMID:日期:2026-01-08ObjectiveThe study aimed to explore the inhibitory effect of stevioside on colorectal cancer and its molecular mechanism.MethodsColorectal cancer cells were selected for functional testing, including the following groups: 0 μM stevioside, 1 μM stevioside, 2.5 μM stevioside and 5 μM stevioside. CCK-8 kit and EdU staining were employed to assess the cell viability. Cell apoptosis was deterred by flow cytometry. Western blot assay was utilized to detect the protein expressions of cleaved-caspase-3, Bax, Bcl-2, E-cadherin and Vimentin. The polarization of macrophage was evaluated through flow cytometry, western blot and immunofluorescence staining. The effect of stevioside on the proliferation of tumor tissue was detected by tumor formation and immunohistochemical staining in nude mice.ResultsStevioside exhibited a significant concentration-dependent inhibitory effect on the proliferation, migration, and invasion of colorectal cancer cells, while promoting apoptosis . Following stevioside treatment, there was a notable reduction in tumor volume and weight observed. Flow cytometry and immunohistochemical staining results showed that compared with control group, CD86+ cell ratio was increased in stevioside treatment group, while the CD206+ cell ratio was decreased in stevioside treatment group. RT-qPCR analysis revealed that, compared to the control group, stevioside treatment significantly reduced the mRNA expressions of Arg-1 and IL-10, while concomitantly increasing the mRNA expressions of IL-12 and TNF-α in a concentration-dependent manner.ConclusionStevioside possesses the ability to significantly hinder the proliferation of colorectal cancer cells and induce apoptosis, the mechanism of which may be closely related to the regulation of macrophage M1 polarization.
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5. Usnic Acid induces dual-pathway apoptosis in SKOV-3 ovarian cancer cells via PARP1 inhibition and MAPK pathway activation.
PMID:日期:2025-12-21IntroductionDue to its silent clinical progression and diagnosis often occurring at advanced stages, ovarian cancer continues to be a major contributor to gynecological cancer-related mortality worldwide. Recent evidence underscores the critical therapeutic value of targeting the interplay between DNA damage response pathways, particularly poly (ADP-ribose) polymerase 1 (PARP1), and mitogen-activated protein kinase (MAPK) signaling cascades.MethodsIn this study, we investigated the anti-cancer potential of the naturally derived small molecule usnic acid in a chemotherapy-resistant epithelial ovarian cancer model (SKOV-3 cells) at the cellular and molecular levels.ResultsOur findings demonstrate for the first time that usnic acid exerts a dual-pathway apoptotic mechanism by simultaneously inhibiting PARP1 and activating the MAPK signaling pathway. Remarkably, usnic acid mimics the gene-silencing action of siRNA on PARP1, suggesting a highly specific and potent inhibitory effect at the molecular level. Although ROS involvement and pathway causality were not directly tested, this dual-action profile enhances DNA damage-induced apoptosis and highlights usnic acid as a promising therapeutic candidate.ConclusionThe study presents a novel molecular framework in which a single small molecule can coordinate apoptosis through parallel regulatory pathways, demonstrating the potential for innovative therapeutic approaches in the treatment of aggressive and treatment-resistant ovarian cancers.
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8. Nickel; a metal with threats to human health, focusing on its intoxication mechanisms.
PMID:日期:2025-12-16Background and ObjectiveNi is an important metal found in the human environment, including air, water, soil, food, kitchenware, and jewelry. It is widely used in electrical engineering, medicine, and industry. Ni compounds, whether insoluble (such as oxides and sulfides) or soluble (such as sulfates, chlorides, and acetates), pose serious risks to the environment, ecosystems, and human health. Such contamination can lead to harmful effects, especially on the respiratory, digestive, and skin systems. This study aims to emphasize the importance of early detection and diagnosis of Ni poisoning, as well as urgent measures and treatments, especially the use of chelators, in addition to the use of nanoparticles to remove nickel compounds from the environment.Methods and ResultThis review article draws on sources from PubMed, Scopus, various citations, and the Toxicologic Emergencies reference book spanning 1996-2025. The findings indicate that high-level exposure to nickel compounds leads to the formation of reactive oxygen species, suppression of DNA repair mechanisms, and disruption of signal transduction pathways. These effects result in genotoxicity, carcinogenicity, immunotoxicity, and poisoning across different species.ConclusionA thorough history and examination are essential for evaluating blood and urine nickel levels, as they directly relate to the severity of poisoning. Preventive measures involve avoiding nickel compounds and facilitating removal from the body. Allergic contact dermatitis is treated with antihistamines, corticosteroids, and calcineurin inhibitors like tacrolimus. For nickel poisoning treatment, chelators such as diethyl-dithiocarbamate (DDC) and disulfiram are prescribed based on urine concentration. Recently, nanoparticles have been used to remove nickel compounds from the environment.