Pub Date : 2026-02-09DOI: 10.1186/s40360-026-01099-y
Yi Jin, Wenyan Zhao, Qian Li, Sunqi Ding, Shuangshuang Tian, Zhaodi Han, Hui Wu, Lu Bai, Hui Liao
{"title":"To investigate the effect of a high-fat diet on pharmacokinetics/renal function/RAAS-related parameters after a single dose of empagliflozin in healthy Chinese adults.","authors":"Yi Jin, Wenyan Zhao, Qian Li, Sunqi Ding, Shuangshuang Tian, Zhaodi Han, Hui Wu, Lu Bai, Hui Liao","doi":"10.1186/s40360-026-01099-y","DOIUrl":"https://doi.org/10.1186/s40360-026-01099-y","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146140649","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 : 2026-02-07DOI: 10.1186/s40360-026-01093-4
Alyssa Steitz, Laura L Daniel, Puran Nepal, Alyson L Dickson, Jacy Zanussi, Tyne W Miller-Fleming, Peter S Straub, Wei-Qi Wei, Ge Liu, Jennifer Maizel, Nancy J Cox, Adriana M Hung, QiPing Feng, C Michael Stein, Cecilia P Chung
{"title":"Association between genetically predicted expression of TPMT and azathioprine adverse events.","authors":"Alyssa Steitz, Laura L Daniel, Puran Nepal, Alyson L Dickson, Jacy Zanussi, Tyne W Miller-Fleming, Peter S Straub, Wei-Qi Wei, Ge Liu, Jennifer Maizel, Nancy J Cox, Adriana M Hung, QiPing Feng, C Michael Stein, Cecilia P Chung","doi":"10.1186/s40360-026-01093-4","DOIUrl":"https://doi.org/10.1186/s40360-026-01093-4","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137314","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 : 2026-01-30DOI: 10.1186/s40360-026-01083-6
Enayatollah Seydi, Sana Ghanizadeh, Farzaneh Jokar, Farzaneh Kamranfar, Jalal Pourahmad
Background: Ketamine exhibits various pharmacological effects due to its high efficacy, but reports also indicate its potential to cause brain side effects and neurotoxicity. It can induce oxidative stress and impair mitochondrial function, although the exact mechanism of its neurotoxicity remains unclear.
Methods: In this study, we examined the effects of α-tocopherol on ketamine-induced toxicity in rat brain neurons. We measured cell viability, ROS levels, membrane damage in mitochondria and lysosomes, and cytochrome c release from mitochondria.
Results: Results showed that ketamine significantly reduced neuron viability, with an IC50 of 4 µM. At concentrations of 2, 4, and 8 µM, ketamine increased ROS production, damaged mitochondrial and lysosomal membranes, and raised cytochrome c release. Notably, α-tocopherol at 10 µM prevented these effects caused by 8 µM ketamine.
Conclusion: It reduced oxidative stress, preserved membrane integrity, and decreased apoptosis signaling, suggesting its potential antioxidant role in counteracting ketamine neurotoxicity.
{"title":"α-tocopherol alleviates ketamine toxicity in rat brain neurons.","authors":"Enayatollah Seydi, Sana Ghanizadeh, Farzaneh Jokar, Farzaneh Kamranfar, Jalal Pourahmad","doi":"10.1186/s40360-026-01083-6","DOIUrl":"https://doi.org/10.1186/s40360-026-01083-6","url":null,"abstract":"<p><strong>Background: </strong>Ketamine exhibits various pharmacological effects due to its high efficacy, but reports also indicate its potential to cause brain side effects and neurotoxicity. It can induce oxidative stress and impair mitochondrial function, although the exact mechanism of its neurotoxicity remains unclear.</p><p><strong>Methods: </strong>In this study, we examined the effects of α-tocopherol on ketamine-induced toxicity in rat brain neurons. We measured cell viability, ROS levels, membrane damage in mitochondria and lysosomes, and cytochrome c release from mitochondria.</p><p><strong>Results: </strong>Results showed that ketamine significantly reduced neuron viability, with an IC<sub>50</sub> of 4 µM. At concentrations of 2, 4, and 8 µM, ketamine increased ROS production, damaged mitochondrial and lysosomal membranes, and raised cytochrome c release. Notably, α-tocopherol at 10 µM prevented these effects caused by 8 µM ketamine.</p><p><strong>Conclusion: </strong>It reduced oxidative stress, preserved membrane integrity, and decreased apoptosis signaling, suggesting its potential antioxidant role in counteracting ketamine neurotoxicity.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092034","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 : 2026-01-28DOI: 10.1186/s40360-026-01092-5
Junyi Zhuo, Hua Wu, Xiaoling Zhou, Xi Wang, Tianqi Qiu, Min Lin, Yu Tang
Background: Ochratoxin A (OTA), a common food-borne mycotoxin, is a potential human carcinogen, yet the specific molecular mechanisms linking it to hepatocellular carcinoma (HCC) remain unclear.
Methods: We integrated network toxicology to predict OTA targets and intersected them with HCC transcriptomic data to identify key candidate genes. Functional enrichment analysis was then conducted. Multiple machine learning algorithms were applied to screen and validate core genes. Furthermore, molecular docking and molecular dynamics (MD) simulations were employed to evaluate the binding stability between OTA and key target proteins.
Results: A total of 50 key genes were identified as potential targets for potential OTA-associated hepatocarcinogenesis. Enrichment analysis revealed their significant involvement in critical processes such as xenobiotic metabolism and oxidative stress response. Machine learning analysis prioritized eight core genes (AURKA, GABARAPL1, CA2, PARP1, LMNA, SLC27A5, EPHX2, and GSTP1), and a combined diagnostic model demonstrated outstanding performance (AUC = 0.986). Structural analyses via molecular docking and MD simulations confirmed stable binding interactions between OTA and these core targets.
Conclusions: This integrated computational study identifies a set of candidate genes through which OTA may potentially interact with HCC-associated molecular networks. The robust binding predicted between OTA and the core targets provides a structural basis for these interactions. These findings offer a prioritized list of targets and a theoretical framework for subsequent experimental validation and investigation into OTA's toxicological role in HCC.
{"title":"Decrypting potential mechanisms linking ochratoxin A to hepatocellular carcinoma: an integrated approach combining toxicology, machine learning, molecular docking, and molecular dynamics simulation.","authors":"Junyi Zhuo, Hua Wu, Xiaoling Zhou, Xi Wang, Tianqi Qiu, Min Lin, Yu Tang","doi":"10.1186/s40360-026-01092-5","DOIUrl":"https://doi.org/10.1186/s40360-026-01092-5","url":null,"abstract":"<p><strong>Background: </strong>Ochratoxin A (OTA), a common food-borne mycotoxin, is a potential human carcinogen, yet the specific molecular mechanisms linking it to hepatocellular carcinoma (HCC) remain unclear.</p><p><strong>Methods: </strong>We integrated network toxicology to predict OTA targets and intersected them with HCC transcriptomic data to identify key candidate genes. Functional enrichment analysis was then conducted. Multiple machine learning algorithms were applied to screen and validate core genes. Furthermore, molecular docking and molecular dynamics (MD) simulations were employed to evaluate the binding stability between OTA and key target proteins.</p><p><strong>Results: </strong>A total of 50 key genes were identified as potential targets for potential OTA-associated hepatocarcinogenesis. Enrichment analysis revealed their significant involvement in critical processes such as xenobiotic metabolism and oxidative stress response. Machine learning analysis prioritized eight core genes (AURKA, GABARAPL1, CA2, PARP1, LMNA, SLC27A5, EPHX2, and GSTP1), and a combined diagnostic model demonstrated outstanding performance (AUC = 0.986). Structural analyses via molecular docking and MD simulations confirmed stable binding interactions between OTA and these core targets.</p><p><strong>Conclusions: </strong>This integrated computational study identifies a set of candidate genes through which OTA may potentially interact with HCC-associated molecular networks. The robust binding predicted between OTA and the core targets provides a structural basis for these interactions. These findings offer a prioritized list of targets and a theoretical framework for subsequent experimental validation and investigation into OTA's toxicological role in HCC.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146060027","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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