Pub Date : 2026-01-24DOI: 10.1186/s40360-025-01077-w
Duncan C Gilbert, Ruth E Langley, Dami Ayadi, Mannab Berhanu, Lakshmi Kowdley Hemanth, Seunghee Kwon, Hossameldin Abdallah, Angela Meade, Noel Clarke, Silke Gillessen, Nicholas James, Gauthier Bouche, Mahesh Parmar, Matthew Nankivell, Laura Murphy
{"title":"Drug re-purposing to improve outcomes in the management of prostate cancer - aims, outcome measures and design of current phase III trials.","authors":"Duncan C Gilbert, Ruth E Langley, Dami Ayadi, Mannab Berhanu, Lakshmi Kowdley Hemanth, Seunghee Kwon, Hossameldin Abdallah, Angela Meade, Noel Clarke, Silke Gillessen, Nicholas James, Gauthier Bouche, Mahesh Parmar, Matthew Nankivell, Laura Murphy","doi":"10.1186/s40360-025-01077-w","DOIUrl":"https://doi.org/10.1186/s40360-025-01077-w","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146043837","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}
{"title":"Mechanistic study of deoxycholic acid in colorectal cancer based on network toxicology and machine learning approaches.","authors":"Yulai Yin, Xueqing Li, Yixuan Xie, Shuang Liu, Shufa Tan, Chen Xu","doi":"10.1186/s40360-026-01091-6","DOIUrl":"https://doi.org/10.1186/s40360-026-01091-6","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008923","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}
{"title":"Compound 7 h exerts its anti-oncogenic effects on colorectal cancer cells by inducing death-receptor-mediated apoptosis, promoting DNA damage, and obstructing autophagic flux.","authors":"Donglin Yang, Yanlai Fu, Jiuhong Huang, Tianzhi Zhang, Hongyi Nie, Yajun Zhang","doi":"10.1186/s40360-026-01087-2","DOIUrl":"https://doi.org/10.1186/s40360-026-01087-2","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008999","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}
Pub Date : 2026-01-16DOI: 10.1186/s40360-025-01081-0
Shu Yang, Lijun Hu, Guohua Liu, Xiaohong Yuan, Xiaoling Chen
{"title":"Development and validation of a nomogram for predicting thrombocytopenia in sepsis patients treated with linezolid.","authors":"Shu Yang, Lijun Hu, Guohua Liu, Xiaohong Yuan, Xiaoling Chen","doi":"10.1186/s40360-025-01081-0","DOIUrl":"https://doi.org/10.1186/s40360-025-01081-0","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988056","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}
Pub Date : 2026-01-16DOI: 10.1186/s40360-026-01088-1
Lava Mohammed Sabir, Hiewa Othman Dyary
Background: Doxorubicin (Dox) is a highly effective chemotherapy drug used to treat various cancers. However, its clinical application is limited by liver toxicity, which is mainly caused by oxidative stress, inflammation, and mitochondrial damage. Myricetin, a natural flavonoid present in many fruits and vegetables, has demonstrated antioxidant and anti-inflammatory activities, making it a potential protective agent against such toxicity.
Methods: This study aimed to evaluate the protective effects of myricetin on Dox-induced liver damage in rats. Thirty-six male Sprague-Dawley rats were divided into six groups: a negative control, a Dox-only group (20 mg/kg, given intraperitoneally on day 10), a myricetin-only group (20 mg/kg, dissolved in corn oil, given orally for 10 days), high-dose (HD) myricetin + Dox (20 mg/kg), low-dose (LD) myricetin + Dox (10 mg/kg), and corn oil control. Biochemical, hematological, oxidative, and histological parameters were evaluated 24 h after Dox injection.
Results: Dox increased serum alanine transaminase (75.6 ± 3.2 U/L), aspartate transaminase (237.6 ± 15.3 U/L), alkaline phosphatase (491.3 ± 16.4 U/L), liver-to-body weight ratio (4.38 ± 0.08%), total oxidant status (TOS, about two-fold compared to the control), and TNF-α (9.94 ± 0.82 U/mL), while decreasing total antioxidant capacity (T-AOC) by 35.2%, and bile acids by 24.0%. Myricetin coadministration, especially at higher doses, significantly reversed these changes. Histopathological evaluation confirmed myricetin's hepatoprotective effect, showing attenuation of hepatocellular degeneration, sinusoidal congestion, and inflammatory infiltration.
Conclusion: Myricetin demonstrated protective effects against Dox-induced liver damage through its antioxidant and anti-inflammatory properties. Further research is warranted.
{"title":"Myricetin protects against doxorubicin-induced liver damage by modulating oxidative and inflammatory pathways.","authors":"Lava Mohammed Sabir, Hiewa Othman Dyary","doi":"10.1186/s40360-026-01088-1","DOIUrl":"10.1186/s40360-026-01088-1","url":null,"abstract":"<p><strong>Background: </strong>Doxorubicin (Dox) is a highly effective chemotherapy drug used to treat various cancers. However, its clinical application is limited by liver toxicity, which is mainly caused by oxidative stress, inflammation, and mitochondrial damage. Myricetin, a natural flavonoid present in many fruits and vegetables, has demonstrated antioxidant and anti-inflammatory activities, making it a potential protective agent against such toxicity.</p><p><strong>Methods: </strong>This study aimed to evaluate the protective effects of myricetin on Dox-induced liver damage in rats. Thirty-six male Sprague-Dawley rats were divided into six groups: a negative control, a Dox-only group (20 mg/kg, given intraperitoneally on day 10), a myricetin-only group (20 mg/kg, dissolved in corn oil, given orally for 10 days), high-dose (HD) myricetin + Dox (20 mg/kg), low-dose (LD) myricetin + Dox (10 mg/kg), and corn oil control. Biochemical, hematological, oxidative, and histological parameters were evaluated 24 h after Dox injection.</p><p><strong>Results: </strong>Dox increased serum alanine transaminase (75.6 ± 3.2 U/L), aspartate transaminase (237.6 ± 15.3 U/L), alkaline phosphatase (491.3 ± 16.4 U/L), liver-to-body weight ratio (4.38 ± 0.08%), total oxidant status (TOS, about two-fold compared to the control), and TNF-α (9.94 ± 0.82 U/mL), while decreasing total antioxidant capacity (T-AOC) by 35.2%, and bile acids by 24.0%. Myricetin coadministration, especially at higher doses, significantly reversed these changes. Histopathological evaluation confirmed myricetin's hepatoprotective effect, showing attenuation of hepatocellular degeneration, sinusoidal congestion, and inflammatory infiltration.</p><p><strong>Conclusion: </strong>Myricetin demonstrated protective effects against Dox-induced liver damage through its antioxidant and anti-inflammatory properties. Further research is warranted.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":"25"},"PeriodicalIF":2.7,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12857104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-14DOI: 10.1186/s40360-025-01059-y
Yuanzhao Xu, Lingyue An, Jiling Xie, Chenggong Luo, Heng Zhang, Qinyi Zhang, Guangheng Luo
<p><strong>Background: </strong>The gut microecosystem represents the most abundant and complex microbial ecosystem in the human body. Maintaining homeostasis of gut microbiota and their metabolites is essential for human health. As a chronic metabolic disorder, the association between benign prostatic hyperplasia (BPH) and gut microbiota remains unclear. Growing evidence suggests that modulating the composition and function of gut microbiota may influence the gut-prostate axis, thereby affecting the development and progression of prostatic hyperplasia. In this study, we employed network pharmacology to systematically elucidate the complex interactions among gut microbiota, microbial metabolites, and BPH-related therapeutic targets.</p><p><strong>Methods: </strong>In this study, we first retrieved information on gut microbial metabolites from the gutMGene database. Subsequently, we identified overlapping targets of these metabolites using the SEA and STP databases. To further clarify targets related to BPH, we integrated data from authoritative databases such as Genecard and OMIM. Based on this information, we constructed a protein-protein interaction (PPI) network to screen for core targets. In addition, we performed systematic GO and KEGG functional enrichment analyses of these targets using the DAVID database. we constructed a network model to illustrate the interactions among microbiota, substrates, metabolites, and targets.Finally, molecular docking validation was performed between the core targets and gut microbiota metabolites.</p><p><strong>Results: </strong>We identified 43 overlapping targets between gut microbial metabolites and BPH. Subsequently, we selected AKT1, IL-6, and IL-1B as core therapeutic targets for BPH. By constructing an MSMT comprehensive network, we found that these three core targets exert therapeutic effects on BPH through interactions with 11 metabolites, 2 substrates, and 4 gut microbial species. Furthermore, GO analysis revealed that gut microbial metabolites influence prostatic hyperplasia by regulating inflammation, immune responses, and the activation of oxidoreductase activity. KEGG analysis indicated that the AGE-RAGE signaling pathway, Toll-like receptor signaling pathway, HIF-1 signaling pathway, C-type lectin receptor signaling pathway, and PI3K/Akt signaling pathway are the major pathways involved in BPH.The molecular docking results demonstrated that butyrate may influence prostatic hyperplasia by modulating the AKT1 gene.</p><p><strong>Discussion: </strong>This study employs a network pharmacology approach to elucidate the intricate "Microbiota-Substrate-Metabolite-Target" (M-S-M-T) network in Benign Prostatic Hyperplasia (BPH), identifying key hub genes (AKT1, IL-6, IL-1B), signaling pathways (PI3K/Akt, AGE-RAGE, HIF-1), and gut microbiota-derived metabolites (butyrate, propionate, TMAO) as central regulators. It further characterizes the functional significance of the Bifidobacterium-tryptophan and Cl
{"title":"Investigating the impact of gut microbiota-derived metabolites on benign prostatic hyperplasia using network pharmacology approaches.","authors":"Yuanzhao Xu, Lingyue An, Jiling Xie, Chenggong Luo, Heng Zhang, Qinyi Zhang, Guangheng Luo","doi":"10.1186/s40360-025-01059-y","DOIUrl":"https://doi.org/10.1186/s40360-025-01059-y","url":null,"abstract":"<p><strong>Background: </strong>The gut microecosystem represents the most abundant and complex microbial ecosystem in the human body. Maintaining homeostasis of gut microbiota and their metabolites is essential for human health. As a chronic metabolic disorder, the association between benign prostatic hyperplasia (BPH) and gut microbiota remains unclear. Growing evidence suggests that modulating the composition and function of gut microbiota may influence the gut-prostate axis, thereby affecting the development and progression of prostatic hyperplasia. In this study, we employed network pharmacology to systematically elucidate the complex interactions among gut microbiota, microbial metabolites, and BPH-related therapeutic targets.</p><p><strong>Methods: </strong>In this study, we first retrieved information on gut microbial metabolites from the gutMGene database. Subsequently, we identified overlapping targets of these metabolites using the SEA and STP databases. To further clarify targets related to BPH, we integrated data from authoritative databases such as Genecard and OMIM. Based on this information, we constructed a protein-protein interaction (PPI) network to screen for core targets. In addition, we performed systematic GO and KEGG functional enrichment analyses of these targets using the DAVID database. we constructed a network model to illustrate the interactions among microbiota, substrates, metabolites, and targets.Finally, molecular docking validation was performed between the core targets and gut microbiota metabolites.</p><p><strong>Results: </strong>We identified 43 overlapping targets between gut microbial metabolites and BPH. Subsequently, we selected AKT1, IL-6, and IL-1B as core therapeutic targets for BPH. By constructing an MSMT comprehensive network, we found that these three core targets exert therapeutic effects on BPH through interactions with 11 metabolites, 2 substrates, and 4 gut microbial species. Furthermore, GO analysis revealed that gut microbial metabolites influence prostatic hyperplasia by regulating inflammation, immune responses, and the activation of oxidoreductase activity. KEGG analysis indicated that the AGE-RAGE signaling pathway, Toll-like receptor signaling pathway, HIF-1 signaling pathway, C-type lectin receptor signaling pathway, and PI3K/Akt signaling pathway are the major pathways involved in BPH.The molecular docking results demonstrated that butyrate may influence prostatic hyperplasia by modulating the AKT1 gene.</p><p><strong>Discussion: </strong>This study employs a network pharmacology approach to elucidate the intricate \"Microbiota-Substrate-Metabolite-Target\" (M-S-M-T) network in Benign Prostatic Hyperplasia (BPH), identifying key hub genes (AKT1, IL-6, IL-1B), signaling pathways (PI3K/Akt, AGE-RAGE, HIF-1), and gut microbiota-derived metabolites (butyrate, propionate, TMAO) as central regulators. It further characterizes the functional significance of the Bifidobacterium-tryptophan and Cl","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145970502","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}
{"title":"Impact of aging on the pharmacokinetic profile of everolimus in male mice.","authors":"Dilek Ozturk Civelek, Ferdi Ozturk, Yasemin Kubra Akyel, Alper Okyar","doi":"10.1186/s40360-025-01079-8","DOIUrl":"https://doi.org/10.1186/s40360-025-01079-8","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145970515","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}
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