Toxicology and applied pharmacology最新文献

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Evaluation of the inhibitory effects of carbamate pesticides on human carboxylesterases 氨基甲酸酯类农药对人羧酸酯酶抑制作用的评价。
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-28 DOI: 10.1016/j.taap.2025.117454
Chen-yuan Liao , Xiao-lei Yi , Yu-xin Yang , Jia-min Gong , Yu-Lin Ma , Fei Long , Zhen-zhong Liu , Zuo Du
{"title":"Evaluation of the inhibitory effects of carbamate pesticides on human carboxylesterases","authors":"Chen-yuan Liao ,&nbsp;Xiao-lei Yi ,&nbsp;Yu-xin Yang ,&nbsp;Jia-min Gong ,&nbsp;Yu-Lin Ma ,&nbsp;Fei Long ,&nbsp;Zhen-zhong Liu ,&nbsp;Zuo Du","doi":"10.1016/j.taap.2025.117454","DOIUrl":"10.1016/j.taap.2025.117454","url":null,"abstract":"<div><div>Carbamate pesticides (CMs), which are widely applied in agricultural production and living environments, have been confirmed to exhibit disruptive effects on lipid metabolism as environmental endocrine disruptors. The present study aims to investigate the inhibition behavior of CMs on the activity of the critical hydrolytic enzymes, carboxylesterase 1 (CES1) and carboxylesterase 2 (CES2), to elucidate the toxicity mechanisms from a novel perspective. Based on network toxicology analysis, CESs were identified as potential targets for CMs-induced lipid metabolism disorders. <em>In vitro</em> incubation experiments demonstrated that most CMs strongly inhibited the activity of CES1 and CES2, with inhibition ratios exceeding 80 %. Kinetic studies and <em>in vitro-in vivo</em> extrapolation revealed that CMs might disrupt the metabolic homeostasis of lipids by inhibiting CESs <em>in vivo</em>. Molecular docking results revealed that hydrogen bonds and hydrophobic contacts formed by ester bonds contributed to the interaction of CMs towards CESs. Cellular fluorescence imaging confirmed the inhibition of CMs on CESs in HepG2 cells. These findings provide new experimental evidence for understanding the mechanism of CMs-mediated lipid metabolism disorders through inhibition on CESs.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"502 ","pages":"Article 117454"},"PeriodicalIF":3.3,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Deguelin inhibits IL-1β-induced chondrocyte inflammation in vitro and ameliorates murine osteoarthritis in vivo Deguelin在体外抑制il -1β诱导的软骨细胞炎症,并在体内改善小鼠骨关节炎。
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-27 DOI: 10.1016/j.taap.2025.117453
Yanben Wang , Jiaqing Ji , Abudureyimu abudukeremu , Dang Ma , Ziyue Yin , Kangshuai Xu , Jian Fan
{"title":"Deguelin inhibits IL-1β-induced chondrocyte inflammation in vitro and ameliorates murine osteoarthritis in vivo","authors":"Yanben Wang ,&nbsp;Jiaqing Ji ,&nbsp;Abudureyimu abudukeremu ,&nbsp;Dang Ma ,&nbsp;Ziyue Yin ,&nbsp;Kangshuai Xu ,&nbsp;Jian Fan","doi":"10.1016/j.taap.2025.117453","DOIUrl":"10.1016/j.taap.2025.117453","url":null,"abstract":"<div><div>Osteoarthritis (OA), a prevalent age-related degenerative joint disorder, is characterized by progressive articular cartilage degradation accompanied by subchondral bone remodeling, synovitis, and reactive osteophytosis. Discovering natural medicines capable of inhibiting inflammatory response of chondrocytes and cartilage degeneration is necessary for OA treatment. Emerging investigations have systematically demonstrated deguelin's multimodal anti-inflammatory efficacy mechanistically across multiple pathological contexts. However, its effect on chondrocytes remains unknown. Through a dual-level investigation combining in vitro mechanistic analysis and in vivo disease modeling, this study delineates deguelin's chondroprotective mechanisms in primary murine chondrocytes, while demonstrating potent disease-modifying effects in surgically induced OA pathogenesis. Deguelin demonstrated significant anti-inflammatory activity in IL-1β-activated chondrocytes. It diminished cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) mRNA and protein levels, and it prevented extracellular matrix (ECM) catabolism by reducing matrix metalloproteinases (MMPs) expression. Mechanistically, deguelin exerted anti-inflammatory effects through targeted suppression of NF-κB pathway activation, as confirmed by immunofluorescence and western blot analyses. Consistent with the in vitro findings, deguelin treatment protected against articular cartilage erosion and subchondral bone loss in OA murine model in vivo, suggesting its potential as an effective agent for treating OA.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"502 ","pages":"Article 117453"},"PeriodicalIF":3.3,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Corrigendum to "Co-delivery of celastrol and lutein with pH sensitive nano micelles for treating acute kidney injury" [Toxicology and Applied Pharmacology Volume 450, 1 September 2022, 116155]. “用pH敏感纳米胶束联合递送celastrol和叶黄素治疗急性肾损伤”的勘误表[毒理学和应用药理学卷450,1 September 2022, 116155]。
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-24 DOI: 10.1016/j.taap.2025.117451
Mengxue Pang, Songchao Duan, Mengmeng Zhao, Qingqing Jiao, Yimeng Bai, Lili Yu, Bin Du, Genyang Cheng
{"title":"Corrigendum to \"Co-delivery of celastrol and lutein with pH sensitive nano micelles for treating acute kidney injury\" [Toxicology and Applied Pharmacology Volume 450, 1 September 2022, 116155].","authors":"Mengxue Pang, Songchao Duan, Mengmeng Zhao, Qingqing Jiao, Yimeng Bai, Lili Yu, Bin Du, Genyang Cheng","doi":"10.1016/j.taap.2025.117451","DOIUrl":"10.1016/j.taap.2025.117451","url":null,"abstract":"","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"117451"},"PeriodicalIF":3.3,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144508420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Effect of parental perinatal exposure to L-glutamate monosodium salt monohydrate on developmental neurotoxicity in rat offspring 父母围产期暴露于l -谷氨酸钠一水合物对大鼠后代发育神经毒性的影响。
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-24 DOI: 10.1016/j.taap.2025.117450
Zizhao Huang , Xiao Xiao , Xuan Zhang , Haijiao Jiang , Xiulan Zhao , Qinzhi Wei , Xingfen Yang , Haixia Sui , Tong Ou , Daoyuan Yang , Weichunbai Zhang , Xudong Jia , Yan Song , Ling Yong
{"title":"Effect of parental perinatal exposure to L-glutamate monosodium salt monohydrate on developmental neurotoxicity in rat offspring","authors":"Zizhao Huang ,&nbsp;Xiao Xiao ,&nbsp;Xuan Zhang ,&nbsp;Haijiao Jiang ,&nbsp;Xiulan Zhao ,&nbsp;Qinzhi Wei ,&nbsp;Xingfen Yang ,&nbsp;Haixia Sui ,&nbsp;Tong Ou ,&nbsp;Daoyuan Yang ,&nbsp;Weichunbai Zhang ,&nbsp;Xudong Jia ,&nbsp;Yan Song ,&nbsp;Ling Yong","doi":"10.1016/j.taap.2025.117450","DOIUrl":"10.1016/j.taap.2025.117450","url":null,"abstract":"<div><div>This study aimed to provide preliminary information about the potential adverse effects of L-Glutamate Monosodium Salt Monohydrate on maternal health and offspring development, particularly about developmental neurotoxicity and abnormal behavior in offspring after oral administration by gavage to female SD rats during the perinatal stage. The study involved administering different doses of L-glutamate monosodium salt monohydrate to four groups, including a vehicle control group. The doses were given orally via gavage from gestation day 6 (GD6) until postnatal day 21 (PND21) at levels of 6000, 3000, and 1000 mg/kg BW. The study found that parental exposure to L-Glutamate Monosodium Salt Monohydrate at a dose of 6000 mg/kg BW had adverse effects on the growth and development of the offspring. These effects included delayed physical development and reflex development. However, no effects on dams were observed. The Lowest Observed Adverse Effect Level (LOAEL) for developmental toxicity to the offspring is 6000 mg/kg BW, and the No Observed Adverse Effect Level (NOAEL) is 3000 mg/kg BW. Additionally, the NOAEL for maternal toxicity is considered to be 6000 mg/kg BW.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"502 ","pages":"Article 117450"},"PeriodicalIF":3.3,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144508421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Elevated SNHG1 promotes invasion and migration of Cd(II)-transformed cells through Sox2, Rac1, and Slug 升高的SNHG1通过Sox2、Rac1和Slug促进Cd(II)转化细胞的侵袭和迁移。
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-24 DOI: 10.1016/j.taap.2025.117452
Zhuo Zhang, Jingxia Li, Daneah Willis, Huailu Tu, Max Costa
{"title":"Elevated SNHG1 promotes invasion and migration of Cd(II)-transformed cells through Sox2, Rac1, and Slug","authors":"Zhuo Zhang,&nbsp;Jingxia Li,&nbsp;Daneah Willis,&nbsp;Huailu Tu,&nbsp;Max Costa","doi":"10.1016/j.taap.2025.117452","DOIUrl":"10.1016/j.taap.2025.117452","url":null,"abstract":"<div><div>Numerous studies have shown that exposure to cadmium [Cd(II)] contributes to the development of cancers in the lung and other organs. Cd(II) compounds are classified as confirmed human carcinogens; however, the mechanisms underlying Cd(II)-induced carcinogenesis remain poorly understood. Small nucleolar RNA host gene 1 (SNHG1), a long non-coding RNA (lncRNA), has been identified as an oncogene. In this study, we investigated the role of SNHG1 in the invasion and migration of Cd(II)-transformed cells. Our findings revealed that SNHG1 expression was significantly elevated in Cd(II)-transformed cells compared to their passage-matched normal BEAS-2B counterparts. Silencing SNHG1 reduced the invasive and migratory capacities of Cd(II)-transformed cells and inhibited malignant transformation induced by long-term Cd exposure. Notably, ectopic expression of SNHG1 alone in BEAS-2B cells was sufficient to drive malignant transformation and enhance invasion and migration, underscoring its oncogenic potential. SRY-box 2 (Sox2), a transcription factor implicated in cancer cell proliferation, invasion, and migration, was found to be upregulated in Cd(II)-transformed cells, while SNHG1 knockdown led to decreased Sox2 protein levels. Similarly, ras-related C3 botulinum toxin substrate 1 (Rac1), a key regulator of cytoskeletal dynamics linked to tumor growth, invasion, and metastasis, was also elevated in Cd(II)-transformed cells. Knockdown of SNHG1 reduced Rac1 protein levels, and Rac1 knockout significantly suppressed invasion and migration. Additionally, we observed increased expression of Slug, a key transcription factor invovlved in epithelial-mesenchymal transition (EMT), and decreased expression of its downstream target E-cadherin in Cd(II)-transformed cells. Collectively, these results demonstrate that elevated SNHG1 promotes the expression of Sox2, Rac1, and Slug, thereby driving the invasive and migratory behavior of Cd(II)-transformed cells.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"502 ","pages":"Article 117452"},"PeriodicalIF":3.3,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144508422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Comparison of in utero phthalate exposure on fetal rat testis transcript and endocrine alterations with apical reproductive alterations in male rats 子宫内邻苯二甲酸酯暴露对雄性大鼠胎鼠睾丸转录和内分泌改变及顶端生殖改变的比较。
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-24 DOI: 10.1016/j.taap.2025.117447
Leon Earl Gray Jr , Christy S. Lambright , Nicola Evans , Jermaine Ford , Justin Conley
{"title":"Comparison of in utero phthalate exposure on fetal rat testis transcript and endocrine alterations with apical reproductive alterations in male rats","authors":"Leon Earl Gray Jr ,&nbsp;Christy S. Lambright ,&nbsp;Nicola Evans ,&nbsp;Jermaine Ford ,&nbsp;Justin Conley","doi":"10.1016/j.taap.2025.117447","DOIUrl":"10.1016/j.taap.2025.117447","url":null,"abstract":"<div><div><em>In utero</em> administration of some diortho phthalate esters (PEs) produces reproductive tract malformations in male and female rat offspring <em>via</em> unknown molecular initiating events. Although the molecular initiating event(s) for these effects are unknown, the PEs consistently alter several key endocrine and gene expression events in the fetal male rat providing a signature of <em>in utero</em> PE exposure. We compared the dose-related alterations of <em>in utero</em> PE exposure on gene expression levels, measured with targeted RT-qPCR custom arrays, and <em>ex vivo</em> testosterone production (T Prod) with the reproductive alterations seen in F1 male rats from three different PE studies. The PEs studied included dicyclohexyl (DCHP) and dipentyl phthalate (DPeP) and a mixture study with five phthalates (DCHP, diethylhexyl (DEHP), dibutyl (DBP), butyl benzyl (BBP), and diisobutyl phthalate (DiBP)). These results demonstrate that targeted testis gene expression and/or T Prod data from short-term prenatal studies conducted during a critical window of fetal masculinization can be used to determine points-of-departure (PODs) for PEs and that these PODs are several fold more protective than the apical effects in postnatal animals. The clear linkage of these gene transcript and testosterone changes to the adverse effects of <em>in utero</em> exposure can facilitate acceptance of the use of gene expression and endocrine data to determine PODs for risk assessment. Furthermore, the use of gene expression and endocrine data from short-term <em>in vivo</em> fetal studies in place of multigenerational reproductive studies for POD determination for PE and mixtures of PEs could increase the rate of POD development for risk assessment and reduce use of animals and other resources.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"502 ","pages":"Article 117447"},"PeriodicalIF":3.3,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144508419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Alisertib inhibits acute myeloid leukemia cell growth by inhibiting STAT3 activation Alisertib通过抑制STAT3激活抑制急性髓系白血病细胞生长
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-20 DOI: 10.1016/j.taap.2025.117449
Pang-Ting Cheng , Ho Lin , Yu-Chiao Cheng , Tzu-Hung Hsiao , Pei-Pei Jhan , Jia-Rung Tsai , Mei-Chih Chen , Tai-Lin Chen , Chieh-Lin Jerry Teng
{"title":"Alisertib inhibits acute myeloid leukemia cell growth by inhibiting STAT3 activation","authors":"Pang-Ting Cheng ,&nbsp;Ho Lin ,&nbsp;Yu-Chiao Cheng ,&nbsp;Tzu-Hung Hsiao ,&nbsp;Pei-Pei Jhan ,&nbsp;Jia-Rung Tsai ,&nbsp;Mei-Chih Chen ,&nbsp;Tai-Lin Chen ,&nbsp;Chieh-Lin Jerry Teng","doi":"10.1016/j.taap.2025.117449","DOIUrl":"10.1016/j.taap.2025.117449","url":null,"abstract":"<div><div>Aurora kinase A (AURKA) plays critical roles in the cell cycle. Its oncogenic functions have been identified in various types of cancer. However, its role in acute myeloid leukemia (AML) has not been extensively explored. Alisertib, a selective AURKA inhibitor, is currently being evaluated in clinical trials for the treatment of several cancers. In this study, we aimed to assess the efficacy of alisertib and elucidate its molecular mechanisms in AML cells. <em>In vitro</em> and <em>in vivo</em> experiments were conducted using western blotting and immunocytochemistry, respectively, to identify the effects of alisertib on two AML cell lines (KG-1 and MOLM-13). Primary cells from three patients with AML were used to examine the response to alisertib treatment. The results showed alisertib significantly reduced Thr288 phosphorylation of AURKA in both KG-1 and MOLM-13 cell lines. Interestingly, it selectively inhibited STAT3 phosphorylation at Tyr705, but not at Ser727. Notably, alisertib significantly decreased interleukin-6-induced nuclear pTyr705-STAT3 levels after short-term treatment, while also affecting the expression of downstream c-Myc. In addition to these <em>in vitro</em> findings, <em>in vivo</em> xenograft model using KG-1 cells showed significant tumor growth retardation accompanied by pTyr705-STAT3 inhibition following alisertib treatment. In primary AML patient cells, we observed a consistent trend in the alisertib-induced reduction of pTyr705-STAT3 and cell growth inhibition. In conclusion, AURKA and alisertib are promising therapeutic targets and treatment options for AML.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"502 ","pages":"Article 117449"},"PeriodicalIF":3.3,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144364628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Telaprevir attenuates caspase-11-dependent pyroptosis in mouse heart following ischemia/reperfusion via inhibition of MALT1/TRAF6 pathway Telaprevir通过抑制MALT1/TRAF6通路减轻小鼠心脏缺血/再灌注后caspase-11依赖性焦亡。
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-20 DOI: 10.1016/j.taap.2025.117448
Ming-Rui Li , Bi-Feng Yao , Can Tang , Xiu-Ju Luo , Jun Peng
{"title":"Telaprevir attenuates caspase-11-dependent pyroptosis in mouse heart following ischemia/reperfusion via inhibition of MALT1/TRAF6 pathway","authors":"Ming-Rui Li ,&nbsp;Bi-Feng Yao ,&nbsp;Can Tang ,&nbsp;Xiu-Ju Luo ,&nbsp;Jun Peng","doi":"10.1016/j.taap.2025.117448","DOIUrl":"10.1016/j.taap.2025.117448","url":null,"abstract":"<div><div>Pyroptosis is one of the major forms of cardiomyocyte death following ischemia/reperfusion (I/R). Mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1)/Tumor necrosis factor receptor associated factor 6 (TRAF6) pathway is involved in cardiomyocyte pyroptosis in mouse heart following I/R, and telaprevir, a hepatitis C virus protease inhibitor, has been predicted as a potential inhibitor of MALT1. This study aims to explore the effect of telaprevir on I/R-induced cardiomyocyte pyroptosis. The C57BL/6J mouse was subjected to 45 min-ischemia plus 24 h-reperfusion to establish the myocardial I/R injury model, while H9c2 cardiomyocytes were exposed to hypoxia for 8 h plus reoxygenation for 24 h (H/R) to simulate the I/R pathological process in vitro. Compared to the control group, pyroptosis was significantly increased in the I/R-treated mouse heart or the H/R-treated cardiomyocytes, evidenced by the elevated GSDMD and caspase-11 cleavage. Compared to the vehicle, telaprevir reduced myocardial infarcted size and cleavage of caspase-11 and gasdermin D (GSDMD) in mouse heart following I/R and cultured cardiomyocytes subjected to H/R in a dose-dependent manner. Mechanistically, telaprevir inhibited the recruitment of TRAF6 by MALT1, concomitant with the reduced recruitment of caspase-11 by TRAF6, and in turn, attenuated caspase-11 K63 poly-ubiquitination and activation, which was further confirmed by knockdown of TRAF6. Based on these results, we concluded that telaprevir could protect mouse heart against I/R injury by reducing caspase-11-dependent pyroptosis through inhibition of MALT1/TRAF6 pathway.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"502 ","pages":"Article 117448"},"PeriodicalIF":3.3,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144369246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
The influence of sexual dimorphism on diaphragm muscle after long-term exposure to e-cigarette 长期接触电子烟后两性异形对横膈肌的影响。
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-19 DOI: 10.1016/j.taap.2025.117446
Ana Beatriz Farias de Souza , Pedro Alves Machado-Junior , Sirlaine Pio , André Talvani , Frank Silva Bezerra
{"title":"The influence of sexual dimorphism on diaphragm muscle after long-term exposure to e-cigarette","authors":"Ana Beatriz Farias de Souza ,&nbsp;Pedro Alves Machado-Junior ,&nbsp;Sirlaine Pio ,&nbsp;André Talvani ,&nbsp;Frank Silva Bezerra","doi":"10.1016/j.taap.2025.117446","DOIUrl":"10.1016/j.taap.2025.117446","url":null,"abstract":"<div><div>Smoking is one of the world's major health problems and is the leading risk factor for chronic obstructive pulmonary disease. Electronic cigarettes (e-cigs) have emerged as an alternative to conventional cigarettes. However, just like cigarette smoke, e-cig aerosols contain toxic compounds that can promote inflammation and oxidative stress. This study evaluated exposure to conventional cigarettes and electronic cigarettes and the effects on the diaphragm muscle of mice of both sexes. Male (<em>n</em> = 24) and female (n = 24) C57BL/6 mice were divided into three groups: control group (C), conventional cigarette group (CC), and electronic cigarette group (<em>E</em>-cig). The animals in the CC and E-cig groups were exposed to the respective cigarettes for 60 days, followed by 60 days without exposure at the end of the experiment; blood and diaphragm were collected for analysis. In blood plasma, females from the e-cig group showed elevated levels of creatine kinase and increased levels of IL-6, IL-12, and IL-10. In the diaphragm muscle, exposure to e-cigs increased total protein levels decreased superoxide dismutase activity and altered catalase activity in males and females. In addition, the levels of TNF, IL-6, and IL-12 were higher in both sexes, while females also showed greater levels of IL-10. Our results suggest that even after a period of recovery, e-cig exposure promotes inflammation and diaphragmatic oxidative stress, and females are more susceptible to the effects of e-cig.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"502 ","pages":"Article 117446"},"PeriodicalIF":3.3,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Corrigendum to "Integrated transcriptomics and metabolomics unravel the key metabolic pathways involved in the therapeutic mechanism of Salvianic acid A against hepatic fibrosis" [Toxicology and Applied Pharmacology 500 (2025) 117398]. “整合转录组学和代谢组学揭示丹参酸A抗肝纤维化治疗机制中涉及的关键代谢途径”[毒理学和应用药理学500(2025)117398]的误读。
IF 3.3 3区 医学
Toxicology and applied pharmacology Pub Date : 2025-06-18 DOI: 10.1016/j.taap.2025.117445
Yunan Zhang, Yan Zhang, Jianan Zhang, Wenfang Lai, Guiqing He, Jichan Shi, Chuan Zhang, Liyan Xiong, Tingfang Wang, Fei Ye, Xiangao Jiang
{"title":"Corrigendum to \"Integrated transcriptomics and metabolomics unravel the key metabolic pathways involved in the therapeutic mechanism of Salvianic acid A against hepatic fibrosis\" [Toxicology and Applied Pharmacology 500 (2025) 117398].","authors":"Yunan Zhang, Yan Zhang, Jianan Zhang, Wenfang Lai, Guiqing He, Jichan Shi, Chuan Zhang, Liyan Xiong, Tingfang Wang, Fei Ye, Xiangao Jiang","doi":"10.1016/j.taap.2025.117445","DOIUrl":"10.1016/j.taap.2025.117445","url":null,"abstract":"","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"117445"},"PeriodicalIF":3.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
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