Human & Experimental Toxicology最新文献_第10页

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IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231192799

引用次数: 0

Treatment with paraquat affects the expression of ferroptosis-related genes. 百草枯会影响铁中毒相关基因的表达。

IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231167585

Xiaogang Ge, Qiqi Cai, Sheng Zhang, Xianlong Wu, Pan Ying, Jingjing Ke, Zhihui Yang

{"title":"Treatment with paraquat affects the expression of ferroptosis-related genes.","authors":"Xiaogang Ge, Qiqi Cai, Sheng Zhang, Xianlong Wu, Pan Ying, Jingjing Ke, Zhihui Yang","doi":"10.1177/09603271231167585","DOIUrl":"https://doi.org/10.1177/09603271231167585","url":null,"abstract":"Objective: We aimed to explore the mechanisms underlying paraquat (PQ)-induced damage using cell lines (NCTC1469, TC-1, TCMK-1) and bioinformatic analysis of the GSE153959 dataset. Assessment of changes in the expression of ferroptosis-related genes in cellular damage due to paraquat poisoning and the important value of these genes in the pathogenesis.Methods: Data were retrieved from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) related to ferroptosis were identified by Venn plots and analyzed for enrichment. Proteins encoded by these DEGs were studied for interactions. qRT-PCR and western blotting analyses of cultured cells were used to determine the expression of ferroptosis-related DEGs and their corresponding protein levels.Results: We identified 25 DEGs primarily involved in epidermal growth factor receptor signaling, apoptotic signaling pathways, endoplasmic reticulum (ER) stress, and ferroptosis. From these, we uncovered eight ferroptosis-related DEGs, four of which were involved in ER response and regulators of ferroptosis-Chac1 (ChaC glutathione specific gamma-glutamylcyclotransferase 1), Atf3 (activating transcription factor 3), Tfrc (transferrin receptor), and Slc7a11 (solute carrier family 7 member 11). Significant changes in mRNA and protein levels of CHAC1, ATF3, TFRC, and SLC7A11 were confirmed in PQ-exposed cells.Conclusion: ER stress and ferroptosis are critical for PQ-induced cell damage. CHAC1, ATF3, TFRC, and SLC7A11 are essential molecules implicated in PQ-induced ferroptosis that may serve as therapeutic targets for the amelioration of PQ poisoning.","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231167585"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9176311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

The possible cytotoxicity and genotoxicity assessment of indaziflam on HepG2 cells. 茚地夫兰对HepG2细胞可能的细胞毒性和遗传毒性评价。

IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231183145

Serpil Könen Adıgüzel

{"title":"The possible cytotoxicity and genotoxicity assessment of indaziflam on HepG2 cells.","authors":"Serpil Könen Adıgüzel","doi":"10.1177/09603271231183145","DOIUrl":"https://doi.org/10.1177/09603271231183145","url":null,"abstract":"The use of pesticides in farmland has increased considerably to protect crops against pests, weeds, and diseases. However, pesticides and/or their residues in ecosystems may affect non-target organisms. Indaziflam is a widely used herbicide in agricultural areas in the southern region of Turkey. Therefore, this study aimed to investigate the possible genotoxic and cytotoxic effects of indaziflam on HepG2 cells using comet assay, micronucleus assay, and xCELLigence. The HepG2 cells were treated with various concentrations of indaziflam for different duration of time based on xCELLigence results. Accordingly, the cells were incubated with indaziflam at final concentrations of 1, 5, 10, 20, 40, and 80 μg/mL for 96 h for cytotoxicity assay. To assess genotoxicity, cells were treated with indaziflam at final concentrations of 10, 40, and 100 μg/mL for 4 and 24 h. Ethanol was used as a solvent for indaziflam. Hydrogen peroxide (40 μM) was used as a positive control. Studies have revealed that indaziflam did not show a statistically cytotoxic effect at the tested doses. Nevertheless, genotoxicity studies showed that indaziflam induced both DNA strand breaks and micronucleus numbers depending on the exposure time and dose.","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231183145"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9626046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Discovery of the mechanism of n-propylparaben-promoting the proliferation of human breast adenocarcinoma cells by activating human estrogen receptors via metabolomics analysis. 代谢组学分析发现n-丙基对羟基苯甲酸酯通过激活人雌激素受体促进人乳腺腺癌细胞增殖的机制。

IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231171648

Yunxia Chen, Chan Zhao, Jun Zheng, Ning Su, Hainan Ji

{"title":"Discovery of the mechanism of n-propylparaben-promoting the proliferation of human breast adenocarcinoma cells by activating human estrogen receptors via metabolomics analysis.","authors":"Yunxia Chen, Chan Zhao, Jun Zheng, Ning Su, Hainan Ji","doi":"10.1177/09603271231171648","DOIUrl":"https://doi.org/10.1177/09603271231171648","url":null,"abstract":"Background: N-propylparaben (PP), a type of paraben, is commonly used as a preservative or antibacterial agent in daily chemicals, medicine, food, cosmetics, feed, and various industrial preservatives. Although PP promotes the growth of human breast adenocarcinoma (MCF-7) cells by activating the human estrogen receptor (ER), the mechanism responsible for this type of programmed cell proliferation is poorly understood.Objective: To clarify the effect of PP on cell metabolic function and the potential molecular mechanism of PP induced MCF-7 cell proliferation from a new perspective.Methods: To use high-resolution mass spectrometry-based metabolomics combined with bioinformatics analysis to analyze the molecular mechanism.Results: The results illustrated that differential endogenous compounds related to the effects of PP on cell metabolic functions were detected. PP was found to promote glycolysis in MCF-7 cells and enhance the tricarboxylic acid cycle (TCA cycle) in mitochondria, thus improving the energy supply to these tumor cells for metabolic function and promotion of rapid proliferation. Moreover, we found that PP promoted cell proliferation by affecting the mitogen-activated protein kinase (MAPK) signaling pathway of MCF-7 cells.Conclusion: Our results revealed the molecular mechanism of low concentration PP promoting MCF-7 cell proliferation by activating ER.","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231171648"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9745140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Beneficial effects of sennoside B on pentylenetetrazole-induced seizures in rats. 番泻皂苷B对戊四唑致大鼠癫痫发作的有益作用。

IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231168764

Hüseyin Sahin, Oytun Erbaş

{"title":"Beneficial effects of sennoside B on pentylenetetrazole-induced seizures in rats.","authors":"Hüseyin Sahin, Oytun Erbaş","doi":"10.1177/09603271231168764","DOIUrl":"https://doi.org/10.1177/09603271231168764","url":null,"abstract":"Background: Epilepsy is a common disorder affecting approximately 50 million people worldwide. Oxidative stress is known to play an important role in the pathophysiology of diseases, including epilepsy. In this study, we investigated the effects of sennoside B on PTZ-induced seizures in rats.Method: The rats were grouped into Group Electroencephalography and Group Behavioral. Both Groups were divided into eight subgroups, and these subgroups were compared in terms of the time of first myoclonic jerk, Racine's Convulsion Scale, malondialdehyde levels, and brain superoxide dismutase activity. The experimental seizure model was performed with pentylenetetrazol.Results: The spike percentage was significantly lower in groups that received sennoside B, and this beneficial effect was shown to be associated with the dose of sennoside B received. The RCS score was lower and the FJM onset time was higher in the sennoside B-administered groups. Additionally, brain MDA and brain aquaporin-3 levels were lower and brain SOD activity was higher in the sennoside-administered groups.Conclusions: The present study shows the beneficial effects of sennoside B on PTZ-induced convulsion in rats. It is considered that sennoside B which is a natural and safe product would be a good candidate for strengthening the management of epilepsy without serious side effects.","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231168764"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9265356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway. 红景天苷通过激活SIRT1/Nrf2通路减轻lps诱导的肾损伤。

IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231169520

Jiaying Pan, Jie Zhu, Liang Li, Tao Zhang, Zhenyu Xu

{"title":"Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway.","authors":"Jiaying Pan, Jie Zhu, Liang Li, Tao Zhang, Zhenyu Xu","doi":"10.1177/09603271231169520","DOIUrl":"https://doi.org/10.1177/09603271231169520","url":null,"abstract":"Background: Salidroside (SAL) is an anti-inflammatory, antioxidant, anticancer, neuroprotective, and renal protective active ingredient extracted from the Chinese herb. Rhodiola Rosea. However, the role of SAL in kidney injury has not yet been elucidated. The study investigates SAL's protective effect and mechanism in lipopolysaccharide (LPS)-induced kidney injury.Methods: Male C57BL/6 wild-type mice (6-8 weeks old) were intraperitoneally injected with 10 mg/kg LPS for 24 h and SAL (50 mg/kg) 2 h before the LPS injection. Biochemical and TUNNEL staining assay analyses were carried out to assess kidney injury. The Elisa assay analyzed the mRNA expression of NGAL and KIM-1. RT-qPCR and Western blotting measured the mRNA and protein expression of HO-1, NQO1, Beclin1, P62, SIRT1, Nrf2, and PNCA, respectively.Results: Our study found that mice co-treated with SAL had significantly reduced blood urea nitrogen (BUN), serum creatinine (Scr), neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1) levels in serum of LPS-induced mice. SAL cotreatment potentially decreased the apoptosis rate of kidney tissue and podocytes induced by LPS. SAL significantly reduced the content of malondialdehyde (MDA) and increased superoxide dismutase (SOD) in LPS-treated mice. Autophagy-related proteins Beclin-1 increased but decreased P62 protein expression by cotreatment of SAL in LPS-injected mice. SAL enhanced the Sirtuin 1 (SIRT1) and nuclear factor erythroid 2-related factor 2 (Nrf2) protein expression in LPS-induced kidney tissues.Conclusion: Our results speculate that SAL protects against LPS-induced kidney injury through activation of the SIRT1/Nrf2 pathway.","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231169520"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Avian riboflavin deficiency causes reliably reproducible peripheral nerve demyelination and, with vitamin supplementation, rapid remyelination. 禽核黄素缺乏会导致可靠的可重复的外周神经脱髓鞘，补充维生素后，会导致快速髓鞘再形成。

IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231188970

Zhao Cai, John Finnie, Jim Manavis, Peter Blumbergs

引用次数: 1

Pulmonary toxicity of sodium dichloroisocyanurate after intratracheal instillation in sprague-dawley rats 气管内灌注二氯异氰尿酸钠对sprague-dawley大鼠的肺毒性

IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2022-05-01 DOI: 10.1177/09603271221106336

Jea-Eun Yoo, Haewon Kim, Yeon-Mi Lim, B. Yoon, P. Kim, I. Eom, Ilseob Shim

{"title":"Pulmonary toxicity of sodium dichloroisocyanurate after intratracheal instillation in sprague-dawley rats","authors":"Jea-Eun Yoo, Haewon Kim, Yeon-Mi Lim, B. Yoon, P. Kim, I. Eom, Ilseob Shim","doi":"10.1177/09603271221106336","DOIUrl":"https://doi.org/10.1177/09603271221106336","url":null,"abstract":"In water, sodium dichloroisocyanurate (NaDCC), a source for chlorine gas generation, releases free available chlorine in the form of hypochlorous acid, a strong oxidizing agent. NaDCC has been used as a disinfectant in humidifiers; however, its inhalation toxicity is a concern. Seven-week-old rats were exposed to NaDCC doses of 100, 500, and 2500 μg·kg−1 body weight by intratracheal instillation (ITI) to investigate pulmonary toxicity. The rats were sacrificed at 1 d (exposure group) or 14 d (recovery group) after ITI. Despite a slight decrease in body weight after exposure, there was no statistically significant difference between the control and NaDCC-treated groups. A significant increase in the total protein level of the bronchoalveolar lavage fluid (BALF) was observed in the exposure groups. Lactate dehydrogenase leakage into the BALF increased significantly (p < 0.01) in the exposure groups; however, recovery was observed after 14 d. The measurement of cytokines in the BALF samples indicated a significant increase in interleukin (IL)-6 in the exposure group and IL-8 in the recovery group. Histopathological examination revealed inflammatory foci and pulmonary edema around the terminal bronchioles and alveoli. This study demonstrated that ITI of NaDCC induced reversible pulmonary edema and inflammation without hepatic involvement in rats.","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"3 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81846315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Antagonism of G protein-coupled receptor 55 prevents lipopolysaccharide-induced damages in human dental pulp cells G蛋白偶联受体55的拮抗作用可预防脂多糖诱导的人牙髓细胞损伤

IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2022-04-01 DOI: 10.1177/09603271221099598

Wei-jie Li, Jie Shen

{"title":"Antagonism of G protein-coupled receptor 55 prevents lipopolysaccharide-induced damages in human dental pulp cells","authors":"Wei-jie Li, Jie Shen","doi":"10.1177/09603271221099598","DOIUrl":"https://doi.org/10.1177/09603271221099598","url":null,"abstract":"Pulpitis is a common oral inflammatory disease in dental pulp commonly associated with bacterial infection. G protein-coupled receptor 55 (GPR55) is a member of the G protein‐coupled receptors family that has been found to regulate inflammatory response. However, its roles in dental pulp inflammation have not been investigated. In this study, we used lipopolysaccharide (LPS) to induce inflammation in human dental pulp cells (hDPCs) to simulate an in vitro model of pulpitis. We found that LPS markedly induced the GPR55 expression in hDPCs. Treatment with the GPR55 antagonist ML-193 ameliorated the LPS-caused decrease in cell viability and increase in lactate dehydrogenase release. The upregulated inflammatory cytokines, interleukin-6 (IL-6) and tumour necrosis factor α, in LPS-challenged hDPCs were also attenuated by ML-193. Treatment with ML-193 ameliorated LPS-induced production of the inflammatory mediators cyclooxygenase-2/prostaglandin E2 (COX-2/PGE2), and inducible nitric oxide synthase/nitric oxide (iNOS/NO) in hDPCs. ML-193 also inhibited the activation of Toll-like receptor 4-myeloid differentiation primary response 88-nuclear factor-κB (TLR4-Myd88-NF-κB) signaling in LPS-induced hDPCs via decreased expressions of TLR4, Myd88, and p-NF-κB 65. Our study provides evidence that the GPR55 antagonist ML-193 exhibited anti-inflammatory activity in LPS-stimulated hDPCs through inhibiting TLR4-Myd88-NF-κB signaling. The results imply that ML-193 might be a novel agent for pulpitis.","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"104 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75941420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Curcumin alleviated lipopolysaccharide-evoked H9c2 cells damage via suppression of intercellular adhesion molecule 1/CD40/NF-κB signaling 姜黄素通过抑制细胞间粘附分子1/CD40/NF-κB信号通路减轻脂多糖诱导的H9c2细胞损伤

IF 2.8 4区医学

Human & Experimental Toxicology Pub Date : 2022-01-01 DOI: 10.1177/09603271211069043

Yi Liu, Xiaoli Li, Yan Zhao

{"title":"Curcumin alleviated lipopolysaccharide-evoked H9c2 cells damage via suppression of intercellular adhesion molecule 1/CD40/NF-κB signaling","authors":"Yi Liu, Xiaoli Li, Yan Zhao","doi":"10.1177/09603271211069043","DOIUrl":"https://doi.org/10.1177/09603271211069043","url":null,"abstract":"Background Curcumin has been reported to have many benefits, including anti-inflammatory, anti-cancer, and so on. In this research, we aimed to investigate the function of curcumin on lipopolysaccharide (LPS)-injured H9c2 cells. Methods H9c2 cells stimulated by LPS mimic the in vitro model of myocarditis injury. Comparative Toxicogenomics Database (CTD) was applied to detect the genes associated with curcumin. GEO database was used to analyze Intercellular Adhesion Molecule 1 (ICAM1) and CD40 expression in myocarditis patients. KEGG enrichment analysis was employed to investigate the meaningful pathways related to differentially expressed genes. Cell proliferation, apoptosis, expression of ICAM1/CD40/P65- NF-κB, and level of TNF-α, IL-6, and IL-10 were observed by cell counting kit-8, flow cytometry and western blotting assays, ELISA assay, respectively. Results After curcumin treatment, the decreased activity of H9c2 cells evoked by LPS was improved. ICAM1 and CD40, which highly expressed in myocarditis patients, were identified as targets of curcumin and negatively regulated by curcumin. Inhibition of ICAM1 or CD40 strengthened the protective effect of curcumin on LPS-evoked H9c2 cells damage, accompanied by increased cell viability and decreased cell apoptosis and inflammation. Additionally, addition of curcumin or depletion of ICAM1/CD40 suppressed p-P65 NF-κB expression. Conclusions Curcumin mitigated LPS-evoked H9c2 cells damage by suppression of ICAM1/CD40/NF-κB, providing a potential molecular mechanism for the clinical application of curcumin.","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"1 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86498995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2