Naglaa Bahr, Abd El-Kader M Abd El-Kader, Alaa Eldin Salah Eldin, Eatemad A Awadalla, Maha A El Demellawy, Doaa A Ghareeb
{"title":"Combined purslane ethanolic extract and metformin attenuate cognitive dysfunction in HFD/STZ-induced diabetic rats via modulation of oxidative stress, neuroinflammation, and neurotransmitters.","authors":"Naglaa Bahr, Abd El-Kader M Abd El-Kader, Alaa Eldin Salah Eldin, Eatemad A Awadalla, Maha A El Demellawy, Doaa A Ghareeb","doi":"10.1186/s40360-026-01128-w","DOIUrl":"10.1186/s40360-026-01128-w","url":null,"abstract":"<p><strong>Background: </strong>Diabetes is associated with a number of significant long-term effects. In this study we consider that purslane which possesses numerous of pharmacological properties, and metformin, an antidiabetic drug, may have a therapeutic effects on diabetes-induced memory impairments in rats.</p><p><strong>Methods: </strong>Forty male albino rats were randomly divided into five groups. Group I served as control group. The other four groups were first fed on HFD followed by a single interpretonial (i.p.) dose of STZ at a dose of (35) mg/kg then the groups were divided as following Group II diabetic group Group III, PEE group administered with oral dose of purslane ethanolic extract (100 mg/kg) for another four weeks. Group IV, MET group administered with oral dose of metformin (100 mg/kg) for another four weeks. Group V (PEE + MET) administered with oral dose of combination of both purslane ethanolic extract (50 mg/kg) and MET (50 mg/kg) for another four weeks. During the treatment rats were tested for memory and learning abilities (Morri's water maze test). Hippocampal samples were collected for biochemical, and histological measurements. Biochemical evaluation included (NO and TBARS) as an oxidative stress marker, (GSH, GPX, SOD, Catalase) as antioxidant, and inflammatory cytokines (tumor necrosis factor-α and interleukin-1β, interleukin-IL-6). Also, P-tau protein, (dopamine and GABA) as neurotransmitters, and for cholinergic system (acetylcholinesterase) were assessed, in addition to histological examinations of hippocampus.</p><p><strong>Results: </strong>Diabetic rats showed a marked cognitive impairment in the Morris water maze test and alteration in the other biochemical and histological features. Intrestingly, PEE and MET treatments partially dramatically enhanced antioxidant levels. Also, reduced oxidative stress, pro-inflammatory mediators, and, phosphorylated tau levels. In addition, PEE and MET treatments partially modulated neurochemical profiles associated with memory function. The combined PEE + MET treatment showed the most pronounced improvement, reflecting synergistic effects. Individual data points highlighted consistent trends across animals. Also, it exhibited a significant restoration of normal hippocampal architecture, as confirmed by hematoxylin and eosin staining.</p><p><strong>Conclusions: </strong>The data obtained indicated that PEE, either alone or in combination with MET, has strong neuroprotective potential against STZ/HFD-induced diabetes. These safeguarding effects are probably because of its strong anti-inflammatory and antioxidant properties.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13141373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810728","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}
Xianghui Zeng, Lihua Wen, Luoying Liu, Qingfeng Zeng, Jianping Luo
{"title":"The potential mechanisms of LCZ696 for anti-hyperthyroid heart disease: an integrative approach of network pharmacology, molecular docking and in vivo verification.","authors":"Xianghui Zeng, Lihua Wen, Luoying Liu, Qingfeng Zeng, Jianping Luo","doi":"10.1186/s40360-026-01145-9","DOIUrl":"https://doi.org/10.1186/s40360-026-01145-9","url":null,"abstract":"<p><strong>Backgroud: </strong>Hyperthyroid heart disease (HHD) is characterized by cardiac remodeling and inflammation, yet targeted therapies remain limited. LCZ696 (sacubitril/valsartan) has demonstrated cardioprotective effects, but its mechanisms in HHD are unclear.</p><p><strong>Methods: </strong>In this study, Network pharmacology alongside experimental validation were employed to elucidate the pharmacological mechanisms of LCZ696 in the treatment of HHD. We identified potential targets for LCZ696 and relevant HHD-related genes from public databases. The mechanisms by which LCZ696 exerts its effects on HHD were further elucidated through GO, KEGG and PPI analysis. The potential molecular targets of LCZ696 were evaluated by molecular docking. Additionally, Echocardiography-measured cardiac function, myocardial fibrosis, target Genes and Inflammatory responses of cardiomyocytes in rat were also examined.</p><p><strong>Results: </strong>A total of 78 target genes for LCZ696 and 1520 HHD targets were obtained. 35 overlapping genes were determined as potential targets of LCZ696 in treating HHD. The PPI analyses highlighted targets being associated with HHD as STAT3, STAT1 and MUC1, suggesting potential binding interactions with LCZ696, as verified by molecular docking analysis, which were also consistent with the experimental results.</p><p><strong>Conclusions: </strong>LCZ696 may ameliorate HHD, potentially associated with reduced inflammation and downregulation of STAT3 signaling.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810743","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}
Fatih Can Turk, Burak Onal, Zulal Celik, Ahmet Gökhan Akkan, Sibel Özyazgan
{"title":"A preliminary investigation of the effects of amentoflavone on TNF-α-induced endothelial activation in HUVECs.","authors":"Fatih Can Turk, Burak Onal, Zulal Celik, Ahmet Gökhan Akkan, Sibel Özyazgan","doi":"10.1186/s40360-026-01143-x","DOIUrl":"https://doi.org/10.1186/s40360-026-01143-x","url":null,"abstract":"<p><strong>Background: </strong>Endothelial dysfunction characterized by cytokine release and adhesion molecule upregulation is a major driver of atherogenesis. Tumor necrosis factor-α (TNF-α) activates NF-κB signaling and increases ICAM-1, VCAM-1, IL-6, and IL-8 expression in endothelial cells. This study aimed to investigate whether amentoflavone (AMF) modulates TNF-α-induced inflammatory and adhesion-related responses in human endothelial cells, supporting its potential to mitigate early vascular dysfunction.</p><p><strong>Methods: </strong>Human umbilical vein endothelial cells (HUVECs) were stimulated with TNF-α (10 ng/mL) in the presence or absence of AMF. Six experimental groups were designed to determine AMF's prophylactic, concurrent, and post-treatment influences on inflammation. Relative mRNA levels of IL-6, IL-8, ICAM-1, VCAM-1, and NF-κB were quantified by qRT-PCR, while protein levels were measured by ELISA.</p><p><strong>Results: </strong>TNF-α markedly increased IL-6, IL-8, ICAM-1, VCAM-1, and NF-κB expression at both the mRNA and protein levels. AMF alone did not trigger any inflammatory response and notably attenuated TNF-α-induced cytokine and adhesion molecule upregulation. Both concurrent and sequential AMF treatments reduced inflammatory responses compared with TNF-α-only cells. Prophylactic AMF administration demonstrated the greatest inhibitory effect, indicating enhanced preventive potential. AMF effectively suppresses TNF-α-mediated endothelial activation by downregulating NF-κB signaling and reducing the expression of IL-6, IL-8, ICAM-1, and VCAM-1.</p><p><strong>Conclusions: </strong>These findings suggest that AMF may represent a promising in vitro preventive candidate against TNF-α-induced endothelial activation, warranting further validation in additional experimental models.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810792","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":"Assessment of the efficiency of new regenerative gel and spray in experimental model systems.","authors":"Natalia Bezdieniezhnykh, Oleksandra Lykhova, Maryna Borshchevska, Andriy Goy, Kyrylo Saulenko, Tamara Kozak, Dmytro Kukurudza, Yevgen Kruglov, Genadiy Borshchevskiy, Liubov Buchynska","doi":"10.1186/s40360-026-01132-0","DOIUrl":"https://doi.org/10.1186/s40360-026-01132-0","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688106","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}
Ufuk Okkay, İlkin Kazimov, Irmak Ferah Okkay, Azizeh Shadidizaji, Mehmet Ali Yoruk, Murat Ozdemir, Fatih Burak Yildiz, Fatma Yesilyurt, Mustafa Ozkaraca, Ahmet Hacimuftuoglu
{"title":"In silico and in vitro insights into the wound-healing potential of syringic acid: protective and regenerative effects on human fibroblasts.","authors":"Ufuk Okkay, İlkin Kazimov, Irmak Ferah Okkay, Azizeh Shadidizaji, Mehmet Ali Yoruk, Murat Ozdemir, Fatih Burak Yildiz, Fatma Yesilyurt, Mustafa Ozkaraca, Ahmet Hacimuftuoglu","doi":"10.1186/s40360-026-01138-8","DOIUrl":"10.1186/s40360-026-01138-8","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13104482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688084","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}
{"title":"Effects of MDMA treatment and cessation on sexual behaviour and testicular functons in male sprague-dawley rats.","authors":"O O Obembe, E T George, R A Mustapha, R E Akhigbe","doi":"10.1186/s40360-026-01131-1","DOIUrl":"https://doi.org/10.1186/s40360-026-01131-1","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147661969","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}