IF 1.2 4区医学

Xenobiotica Pub Date : 2025-10-07 DOI: 10.1080/00498254.2025.2566205

Rongqi Ma, Jiyu Gong, Xiaoyan Xie, Shuyun Liang, Zizhao Yang, Jiannan Li

{"title":"Mechanism of Black American Ginseng saponins in ameliorating memory dysfunction in aging mice by activating the BDNF/PI3K/AKT/CREB pathway.","authors":"Rongqi Ma, Jiyu Gong, Xiaoyan Xie, Shuyun Liang, Zizhao Yang, Jiannan Li","doi":"10.1080/00498254.2025.2566205","DOIUrl":"10.1080/00498254.2025.2566205","url":null,"abstract":"Black American Ginseng (Panax quinquefolium L.) is a traditional Chinese medicine taken orally. While saponins from American Ginseng are known to enhance memory, the effects and mechanisms of Black American Ginseng saponins remain unclear.This study investigates their potential in alleviating memory impairment in ageing mice. UPLC-Q-Orbitrap-MS/MS was used to identify compounds in Black American Ginseng, and network pharmacology predicted potential targets. The Morris water maze test assessed cognitive function, while Western blot and ELISA measured BDNF, TrkB, inflammatory markers (IL-1β, TNF-α, IL-6), and the activation of the PI3K/AKT/CREB signalling pathway. Networking pharmacology and PPI analysis identified PIK3CA, EGFR, and PIK3R1 as key targets, with KEGG enrichment highlighting the PI3K/AKT pathway. Behavioural tests confirmed that Black American Ginseng saponins significantly improved memory in ageing mice. Molecular analyses revealed upregulation of BDNF and TrkB and suppression of IL-1β and IL-6. Additionally, Western blot confirmed activation of the PI3K/AKT/CREB pathway, supporting its neuroprotective role.Black American Ginseng saponins enhance cognitive function by modulating neurotrophic signalling and reducing neuroinflammation.These findings provide new insights into their potential therapeutic application for age-related cognitive decline.","PeriodicalId":23812,"journal":{"name":"Xenobiotica","volume":" ","pages":"1-19"},"PeriodicalIF":1.2,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233713","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

The acute effect of glyphosate on heart mitochondria does not impair the bioenergetics. 草甘膦对心脏线粒体的急性作用不影响生物能量学。

IF 1.2 4区医学

Xenobiotica Pub Date : 2025-10-06 DOI: 10.1080/00498254.2025.2568631

Antonia Cugliari, Cristina Algieri, Micaela Fabbri, Fabiana Trombetti, Giulia Rampazzo, Teresa Gazzotti, Giampiero Pagliuca, Salvatore Nesci

引用次数: 0

Protective effect of carvacrol in a cardiac myoblast cell model of myocardial ischemia-reperfusion injury. carvacrol对心肌缺血再灌注损伤成肌细胞模型的保护作用。

IF 1.2 4区医学

Xenobiotica Pub Date : 2025-10-01 DOI: 10.1080/00498254.2025.2567470

Ali M Albarrati, Rakan I Nazer

{"title":"Protective effect of carvacrol in a cardiac myoblast cell model of myocardial ischemia-reperfusion injury.","authors":"Ali M Albarrati, Rakan I Nazer","doi":"10.1080/00498254.2025.2567470","DOIUrl":"https://doi.org/10.1080/00498254.2025.2567470","url":null,"abstract":"Phytopharmacology has become a key approach for developing new therapeutic strategies by utilizing the diverse bioactive properties of plant-derived compounds to treat complex diseases, including cardiovascular disorders.Myocardial ischemia-reperfusion (I/R) injury presents a major challenge in the management of acute myocardial infarction by worsening myocardial damage through oxidative stress, apoptosis, and cellular senescence.Carvacrol, a monoterpenoid phenol present in plants such as Origanum vulgare, possesses potent antioxidant and anti-inflammatory properties.This study investigates carvacrol's cardioprotective effects in an H9C2 cardiac myoblast model of I/R injury.Cardiac myoblast cells were exposed to an ischemic buffer to simulate I/R conditions, with carvacrol administered at a sub-cytotoxic dose of 12.5 µg/ml prior to exposure. Carvacrol significantly enhanced cell viability by 77.37% restoration, reduced lactate dehydrogenase (LDH) release (from 330.5 ± 25.3 to 160.8 ± 15.7 U/ml, p < 0.01), suppressed reactive oxygen species (ROS) production, inhibited caspase-3 and -8 activities, and mitigated cellular senescence as evidenced by reduced β-galactosidase staining. Additionally, carvacrol restored the expression of the myogenin gene, which was downregulated by ischemic injury.These findings highlight carvacrol's antioxidant, anti-apoptotic, anti-senescence, and gene-regulatory properties, positioning it as a promising therapeutic candidate for mitigating myocardial I/R injury.","PeriodicalId":23812,"journal":{"name":"Xenobiotica","volume":" ","pages":"1-12"},"PeriodicalIF":1.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201764","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

Fluoxetine as an antidepressant agent induces directly deleterious effects on rat isolated pancreatic mitochondria: ameliorative role of betanin. 氟西汀作为抗抑郁剂对大鼠离体胰腺线粒体的直接有害作用：甜菜素的改善作用。

IF 1.2 4区医学

Xenobiotica Pub Date : 2025-09-29 DOI: 10.1080/00498254.2025.2564120

Ahmad Salimi, Saleh Khezri, Amir Mohsen Azami, Samin Tayefeh Ayremlou, Vahed Adhami

{"title":"Fluoxetine as an antidepressant agent induces directly deleterious effects on rat isolated pancreatic mitochondria: ameliorative role of betanin.","authors":"Ahmad Salimi, Saleh Khezri, Amir Mohsen Azami, Samin Tayefeh Ayremlou, Vahed Adhami","doi":"10.1080/00498254.2025.2564120","DOIUrl":"10.1080/00498254.2025.2564120","url":null,"abstract":"It has been shown that fluoxetine is cytotoxic on pancreatic beta-cells via induction of mitochondrial dysfunction and oxidative stress. We investigated the direct effect of fluoxetine on isolated pancreatic mitochondria and evaluate the potential protective effects of betanin and thymoquinone.Mitochondria were isolated from rat pancreas and treated with various concentrations of fluoxetine (10-8000 µM). Then, protective effect of betanin (100-500 µM) and thymoquinone (10-100 µM) on fluoxetine-induced mitochondrial toxicity were studied (60 min). The activity of succinate dehydrogenases (SDH), reactive oxygen species (ROS) formation, mitochondrial swelling, mitochondrial membrane potential (MMP) collapse, malondialdehyde (MDA) production and glutathione level were analysed.Fluoxetine directly caused toxicity in pancreatic isolated mitochondria at concentration of 500 μM and higher. Except MDA and GSH, fluoxetine caused significantly SDH activity reduction, MMP collapse, mitochondrial swelling and ROS formation in pancreatic mitochondria. However, our results showed that only betanin protected fluoxetine-induced mitochondrial dysfunction, while thymoquinone had no impact on mitochondrial toxicity induced by fluoxetine.We can conclude that fluoxetine is directly toxic on pancreas isolated mitochondria, which may be related to its diabetogenic potential in humans. Moreover, our finding suggested that use of betanin may be beneficial for prevention of diabetogenic effect of fluoxetine.","PeriodicalId":23812,"journal":{"name":"Xenobiotica","volume":" ","pages":"1-11"},"PeriodicalIF":1.2,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145132030","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

Apigenin Derivatives as Promising Norovirus RdRp Inhibitors: Insights from In Silico Docking and Molecular Dynamics Studies. 芹菜素衍生物作为有前途的诺如病毒RdRp抑制剂：来自硅对接和分子动力学研究的见解。

IF 1.2 4区医学

Xenobiotica Pub Date : 2025-09-26 DOI: 10.1080/00498254.2025.2566212

M D Sanober, Estari Mamidala

{"title":"Apigenin Derivatives as Promising Norovirus RdRp Inhibitors: Insights from In Silico Docking and Molecular Dynamics Studies.","authors":"M D Sanober, Estari Mamidala","doi":"10.1080/00498254.2025.2566212","DOIUrl":"https://doi.org/10.1080/00498254.2025.2566212","url":null,"abstract":"Norovirus is a leading cause of acute gastroenteritis worldwide, yet no approved antivirals currently exist. In this study, we employed in silico approaches to evaluate apigenin derivatives as potential inhibitors of norovirus RNA-dependent RNA polymerase (RdRp). Seventy-three compounds were initially retrieved from the ZINC database, of which 36 satisfied Lipinski's Rule of Five and were advanced for detailed analysis. Pharmacokinetic predictions revealed high intestinal absorption and favorable drug-likeness profiles for most derivatives, with limited central nervous system penetration, desirable for targeting gastrointestinal infections. Molecular docking identified ZINC14636470 (A1) as the top candidate with strong binding affinity (-9.9 kcal/mol) and key hydrogen bond interactions at the RdRp active site. Molecular dynamics simulations confirmed the stability of the A1-RdRp complex (RMSD = 0.20 ± 0.03 nm; Rg = 2.39 ± 0.02 nm). While AMES predictions flagged some derivatives as potentially mutagenic, scaffold optimization may mitigate these risks. Apigenin derivatives, particularly A1, demonstrate promising inhibitory potential against norovirus RdRp, combining favorable pharmacokinetic properties with stable enzyme binding. These findings provide a computational foundation for subsequent in vitro and in vivo validation, supporting the development of natural flavonoid-based scaffolds as antiviral leads against norovirus.","PeriodicalId":23812,"journal":{"name":"Xenobiotica","volume":" ","pages":"1-16"},"PeriodicalIF":1.2,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145151196","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

Aloe-emodin regulates colon epithelial cell function by regulating HIF-1α to alleviate irritable bowel syndrome. 芦荟大黄素通过调节HIF-1α调节结肠上皮细胞功能减轻肠易激综合征。

IF 1.2 4区医学

Xenobiotica Pub Date : 2025-09-21 DOI: 10.1080/00498254.2025.2559959

Qinghua Wang, Shiyu Lu, Zhonghao Yin

{"title":"Aloe-emodin regulates colon epithelial cell function by regulating HIF-1α to alleviate irritable bowel syndrome.","authors":"Qinghua Wang, Shiyu Lu, Zhonghao Yin","doi":"10.1080/00498254.2025.2559959","DOIUrl":"10.1080/00498254.2025.2559959","url":null,"abstract":"This study aimed to investigate the therapeutic potential of Aloe-emodin (AE) for irritable bowel syndrome (IBS), focusing on its effects and underlying mechanisms.Deoxycholic acid (DCA)-induced IBS rats (Sprague-Dawley) were orally administered AE. Body weight and faecal pellet were monitored. Anxiety-like behaviour, visceral hypersensitivity, colon permeability were assessed via the open-field (OF) test, abdominal Withdrawal Reflex (AWR) score, FITC-dextran fluorescence, respectively. Enzyme-linked immunosorbent assay (ELISA) quantified substance P (SP), 5-hydroxytryptamine (5-HT), TNF-α, and IL-6 levels. Hypoxia inducible factor-1α (HIF-1α) expression was analysed via qRT-PCR. The mechanism of AE on IBS was evaluated in LPS-treated NCM460 injury.AE alleviated IBS symptoms (improved weight gain, reduced faecal output/water content, increased centre exploration time, lowered AWR scores, decreased colon permeability, SP, 5-HT, and pro-inflammatory cytokine levels). HIF-1α upregulation in colonic tissues and LPS-induced NCM460 cells was suppressed by AE treatment. The protective effect of AE was reversed by HIF-1α overexpression in IBS rats. AE enhanced cell proliferation, reduced cellular permeability, and inflammation in LPS-stimulated NCM460 cells. HIF-1α overexpression partially reversed the protective effects of AE in LPS-induced NCM460 injury.AE ameliorated IBS symptoms by promoting cell proliferation, suppressing cell permeability, and inflammation of colonic epithelial cells via regulating HIF-1α.","PeriodicalId":23812,"journal":{"name":"Xenobiotica","volume":" ","pages":"1-11"},"PeriodicalIF":1.2,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145034181","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

Calycosin improves insulin resistance by regulating the hsa-miR-324-3p/AKT pathway to inhibit FOXO3a nuclear transfer. 毛蕊异黄酮通过调节hsa-miR-324-3p/AKT通路抑制FOXO3a核转移来改善胰岛素抵抗。

IF 1.2 4区医学

Xenobiotica Pub Date : 2025-09-18 DOI: 10.1080/00498254.2025.2558648

Junling Zhu, Rilian Lai, Qin Zheng, Shuying Huang, Shenghua Hu, Zhangfei Xu, Huixia Sun

{"title":"Calycosin improves insulin resistance by regulating the hsa-miR-324-3p/AKT pathway to inhibit FOXO3a nuclear transfer.","authors":"Junling Zhu, Rilian Lai, Qin Zheng, Shuying Huang, Shenghua Hu, Zhangfei Xu, Huixia Sun","doi":"10.1080/00498254.2025.2558648","DOIUrl":"10.1080/00498254.2025.2558648","url":null,"abstract":"1. To study the effects of calycosin on palmitic acid-induced HepG2 cells, as well as the potential mechanisms of action.2. Potential targets of calycosin for the alleviation of insulin resistance were predicted by network pharmacology. Glucose concentration in the culture medium was determined by the GOD-POD method. The model of insulin resistance was established by palmitic acid-induced HepG2 cells. Effects of palmitic acid and calycosin on HepG2 cell activity were determined using an MTT assay kit. The expression levels of AKT1 and FOXO3a were detected by western blot. The expression level of hsa-miR-324-3p was detected by RT-qPCR. Dual luciferase reporter assay to detect targeting of AKT1 by hsa-miR-324-3p.3. AKT1 was predicted and validated as a potential target of calycosin for treatment of insulin resistance. The model of insulin resistance was successfully established by palmitic acid-induced HepG2 cells. Up-regulation of AKT1 expression inhibits FOXO3a entry into the nucleus. Calycosian was demonstrated to concentration-dependently increase the sensitivity of insulin resistance cells to insulin. The hsa-miR-324-3p was proven to exist in insulin-resistant cells. Hsa-miR-324-3p was found to target AKT1 involved in the alleviation of insulin resistance.4. Calycosin inhibits FOXO3a nuclear translocation by regulating the hsa-miR-324-3p/AKT pathway, thus alleviating insulin resistance.","PeriodicalId":23812,"journal":{"name":"Xenobiotica","volume":" ","pages":"1-9"},"PeriodicalIF":1.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145030731","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

Analysis of the therapeutic potential of astragalin: insights into target interactions and mechanisms. 黄芪黄芪苷的治疗潜力分析：对靶标相互作用和机制的见解。

IF 1.2 4区医学

Xenobiotica Pub Date : 2025-09-18 DOI: 10.1080/00498254.2025.2559962

Hai Duc Nguyen

{"title":"Analysis of the therapeutic potential of astragalin: insights into target interactions and mechanisms.","authors":"Hai Duc Nguyen","doi":"10.1080/00498254.2025.2559962","DOIUrl":"10.1080/00498254.2025.2559962","url":null,"abstract":"Astragalin (AST), a flavonoid, shows promise for neurodegenerative diseases like Parkinson's disease (PD), cognitive impairment (CI), and depression. However, its efficacy in treating neurodegenerative diseases and the underlying molecular mechanisms remain unclear.This study aims to evaluate the metabolite profile, pharmacokinetics, toxicity, molecular targets, and potential biological activities of AST. Thirty-one AST metabolites formed through Phase II reactions (O-glucuronidation, O-sulfation, and methylation) were found.AST and its metabolites partially violate Lipinski's Rule of Five, including molecular weight and hydrogen bond donors, impacting drug-likeness. However, AST and its metabolites have favourable safety and potential anti-neurodegenerative and antidepressant effects.AST shows strong binding affinities with key neuroinflammatory targets, including IL1B, IL6, TNF, NOS2, PTGS2, SERT, caspase-3, caspase-8, and GABAa receptor, and network analysis highlights its association with neuroinflammatory pathways.Collectively, these findings support AST as a potential neurotherapeutic candidate and offer a basis for further in vitro and in vivo validation.","PeriodicalId":23812,"journal":{"name":"Xenobiotica","volume":" ","pages":"1-20"},"PeriodicalIF":1.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145041500","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

Cytotoxic effects of flurbiprofen on rat adipose-derived stem cells. 氟比洛芬对大鼠脂肪干细胞的细胞毒性作用。

IF 1.2 4区医学

Xenobiotica Pub Date : 2025-09-03 DOI: 10.1080/00498254.2025.2552250

Jiamin Zeng, Xinyao Zhang, Lili Long, Beini Tan, Minghui Zhong, Fanwen Yang, Shicong Zheng, Zhe Yang, Fengyi Zhang, Lan Lan, Sida Liao

{"title":"Cytotoxic effects of flurbiprofen on rat adipose-derived stem cells.","authors":"Jiamin Zeng, Xinyao Zhang, Lili Long, Beini Tan, Minghui Zhong, Fanwen Yang, Shicong Zheng, Zhe Yang, Fengyi Zhang, Lan Lan, Sida Liao","doi":"10.1080/00498254.2025.2552250","DOIUrl":"10.1080/00498254.2025.2552250","url":null,"abstract":"Adipose-derived stem cells (ADSCs) offer a novel approach for treating orthopaedic diseases. Flurbiprofen is a non-steroidal anti-inflammatory analgesic drug used in bone injury therapy. However, its cytotoxicity to ADSCs remains unclear.The differentiation potential of ADSCs was analysed in vitro using the differentiation induction method. Microscopic analysis, Live/Dead staining, MTT assay, and CCK8 assay were used to determine the cytotoxic effects of flurbiprofen on ADSCs at different concentration gradients. Vascular endothelial growth factor (VEGF) levels were measured by ELISA to reflect flurbiprofen's effects on the activity and paracrine function of ADSCs. ANOVA was applied, with p < 0.05 considered significant and p < 0.01 highly significant.Live cell concentration decreased dose-dependently with flurbiprofen treatment, particularly on the 7th day. The level of VEGF decreased significantly with the increase of the concentration of flurbiprofen in a certain concentration range, which indicated that flurbiprofen could inhibit the activity and secreted proteins of ADSCs.Our study showed that small doses of flurbiprofen did not affect the secretion of proteins by cells and cell activity. Therefore, it is necessary to pay attention to the concentration of flurbiprofen in the clinical application of ADSCs therapy for orthopaedic diseases.","PeriodicalId":23812,"journal":{"name":"Xenobiotica","volume":" ","pages":"1-11"},"PeriodicalIF":1.2,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144971404","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

Permethrin disrupts antioxidant defense responses in Litopenaeus vannamei. 氯菊酯破坏凡纳滨对虾的抗氧化防御反应。

IF 1.2 4区医学

Xenobiotica Pub Date : 2025-07-01 Epub Date: 2025-09-02 DOI: 10.1080/00498254.2025.2538539

Juliana Righetto Moser, Eliziane Silva, Maria Risoleta Freire Marques

引用次数: 0

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