{"title":"α-苦叶酚和β-苦叶酚对二乙基亚硝胺所致急性脑损伤的改善作用","authors":"Gulsah Yildiz Deniz , Fatime Geyikoglu","doi":"10.1016/j.toxicon.2025.108550","DOIUrl":null,"url":null,"abstract":"<div><div>Diethylnitrosamine (DEN) is a widely distributed environmental pollutant known for its toxicity and carcinogenicity in various animal species. The aim of the study was to investigate the neuroprotective effects of α-eudesmol and β-eudesmol against DEN-induced brain damage in rats. Sprague-Dawley rats received a single intraperitoneal dose of DEN (200 mg/kg), followed by intravenous administration of α-eudesmol or β-eudesmol (1 mg/kg) three times weekly for 21 days. Brain tissues were collected for histological, biochemical, and immunohistochemical analyses, including markers of brain injury (c-fos) and apoptosis (caspase 3). DEN exposure significantly decreased antioxidant enzyme activities (catalase, glutathione peroxidase, and superoxide dismutase) and increased oxidative stress marker malondialdehyde. It also triggered platelet activation, inflammatory cytokine production, and pathological changes in brain tissue, accompanied by upregulated c-fos and caspase 3 expression. Treatment with α-eudesmol and β-eudesmol effectively mitigated these alterations by modulating the NF-κB/COX-2/TNF-α/IL-6 signaling pathways and restoring dopamine levels to near control values. These findings highlight the potential of α-eudesmol and β-eudesmol as therapeutic agents against DEN-induced neurotoxicity.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"266 ","pages":"Article 108550"},"PeriodicalIF":2.4000,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Amelioration of diethylnitrosamine-induced acute brain injury by α-eudesmol and β-eudesmol\",\"authors\":\"Gulsah Yildiz Deniz , Fatime Geyikoglu\",\"doi\":\"10.1016/j.toxicon.2025.108550\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Diethylnitrosamine (DEN) is a widely distributed environmental pollutant known for its toxicity and carcinogenicity in various animal species. The aim of the study was to investigate the neuroprotective effects of α-eudesmol and β-eudesmol against DEN-induced brain damage in rats. Sprague-Dawley rats received a single intraperitoneal dose of DEN (200 mg/kg), followed by intravenous administration of α-eudesmol or β-eudesmol (1 mg/kg) three times weekly for 21 days. Brain tissues were collected for histological, biochemical, and immunohistochemical analyses, including markers of brain injury (c-fos) and apoptosis (caspase 3). DEN exposure significantly decreased antioxidant enzyme activities (catalase, glutathione peroxidase, and superoxide dismutase) and increased oxidative stress marker malondialdehyde. It also triggered platelet activation, inflammatory cytokine production, and pathological changes in brain tissue, accompanied by upregulated c-fos and caspase 3 expression. Treatment with α-eudesmol and β-eudesmol effectively mitigated these alterations by modulating the NF-κB/COX-2/TNF-α/IL-6 signaling pathways and restoring dopamine levels to near control values. These findings highlight the potential of α-eudesmol and β-eudesmol as therapeutic agents against DEN-induced neurotoxicity.</div></div>\",\"PeriodicalId\":23289,\"journal\":{\"name\":\"Toxicon\",\"volume\":\"266 \",\"pages\":\"Article 108550\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2025-08-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicon\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0041010125003253\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PHARMACOLOGY & PHARMACY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicon","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0041010125003253","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
Amelioration of diethylnitrosamine-induced acute brain injury by α-eudesmol and β-eudesmol
Diethylnitrosamine (DEN) is a widely distributed environmental pollutant known for its toxicity and carcinogenicity in various animal species. The aim of the study was to investigate the neuroprotective effects of α-eudesmol and β-eudesmol against DEN-induced brain damage in rats. Sprague-Dawley rats received a single intraperitoneal dose of DEN (200 mg/kg), followed by intravenous administration of α-eudesmol or β-eudesmol (1 mg/kg) three times weekly for 21 days. Brain tissues were collected for histological, biochemical, and immunohistochemical analyses, including markers of brain injury (c-fos) and apoptosis (caspase 3). DEN exposure significantly decreased antioxidant enzyme activities (catalase, glutathione peroxidase, and superoxide dismutase) and increased oxidative stress marker malondialdehyde. It also triggered platelet activation, inflammatory cytokine production, and pathological changes in brain tissue, accompanied by upregulated c-fos and caspase 3 expression. Treatment with α-eudesmol and β-eudesmol effectively mitigated these alterations by modulating the NF-κB/COX-2/TNF-α/IL-6 signaling pathways and restoring dopamine levels to near control values. These findings highlight the potential of α-eudesmol and β-eudesmol as therapeutic agents against DEN-induced neurotoxicity.
期刊介绍:
Toxicon has an open access mirror Toxicon: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. An introductory offer Toxicon: X - full waiver of the Open Access fee.
Toxicon''s "aims and scope" are to publish:
-articles containing the results of original research on problems related to toxins derived from animals, plants and microorganisms
-papers on novel findings related to the chemical, pharmacological, toxicological, and immunological properties of natural toxins
-molecular biological studies of toxins and other genes from poisonous and venomous organisms that advance understanding of the role or function of toxins
-clinical observations on poisoning and envenoming where a new therapeutic principle has been proposed or a decidedly superior clinical result has been obtained.
-material on the use of toxins as tools in studying biological processes and material on subjects related to venom and antivenom problems.
-articles on the translational application of toxins, for example as drugs and insecticides
-epidemiological studies on envenoming or poisoning, so long as they highlight a previously unrecognised medical problem or provide insight into the prevention or medical treatment of envenoming or poisoning. Retrospective surveys of hospital records, especially those lacking species identification, will not be considered for publication. Properly designed prospective community-based surveys are strongly encouraged.
-articles describing well-known activities of venoms, such as antibacterial, anticancer, and analgesic activities of arachnid venoms, without any attempt to define the mechanism of action or purify the active component, will not be considered for publication in Toxicon.
-review articles on problems related to toxinology.
To encourage the exchange of ideas, sections of the journal may be devoted to Short Communications, Letters to the Editor and activities of the affiliated societies.