Toxicon最新文献

{"title":"Arthrogryposis and axonopathy in the spinal cord in offspring of beef cattle grazing regrowth Sorghum spp. in Brazil","authors":"Ana Lívia Vasconcelos de Sousa ,&nbsp;Davi Emanuel Ribeiro de Sousa ,&nbsp;Cintia Regina Rêgo Queiroz-Machado ,&nbsp;Isabeli Joaquim Contel ,&nbsp;Alessandre Hataka ,&nbsp;Müller Carrara Martins ,&nbsp;Anderson Saravia ,&nbsp;Edson Moleta Colodel ,&nbsp;Aníbal G. Armién ,&nbsp;Franklin Riet-Correa ,&nbsp;Márcio Botelho de Castro ,&nbsp;Mizael Machado","doi":"10.1016/j.toxicon.2025.108439","DOIUrl":"10.1016/j.toxicon.2025.108439","url":null,"abstract":"<div><div>Sorghum-associated arthrogryposis and axonopathy is a rare congenital condition reported in ruminants and horses. Here, we describe the epidemiologic, clinical, and pathologic aspects of nine outbreaks of this condition in beef cattle in midwestern and southeastern Brazil (2014–2023). These regions are the most productive grain sorghum areas, where livestock producers use the straw extensively, producing a high regrowth during drought periods. All the affected pregnant cows had grazed sorghum stover for periods ranging from 25 days to 4 months. They showed abortion in the final and middle third of gestation or gave birth to calves with arthrogryposis, with overflexion or overextension of the limbs. No other gross lesions were observed. Typical neurohistologic lesions in four autopsied calves from different outbreaks included scarce to numerous axonal spheroids in the gray matter of the dorsal and ventral horns in the cervical spinal cord. Ultrastructurally, degenerated axons exhibited a segmental accumulation of residual bodies and degenerate organelles. The combination of sorghum stover consumption by the dams and characteristic spinal cord lesions in affected calves is distinctive and confirms the diagnosis. Sorghum consumption in the region was also associated with acute poisoning and cystitis-ataxia syndrome. For the first time in the Americas, we report a sorghum-associated congenital syndrome characterized by arthrogryposis and axonopathy in beef cattle.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"264 ","pages":"Article 108439"},"PeriodicalIF":2.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144221759","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}

{"title":"Latrodectus spp. toxins outside venom glands: past, present and future","authors":"Xianchun Wang","doi":"10.1016/j.toxicon.2025.108437","DOIUrl":"10.1016/j.toxicon.2025.108437","url":null,"abstract":"<div><div><em>Latrodectus</em> spp. are one of the highly poisonous spiders known in the world. Interestingly, the spiders not only produce and secrete toxins by their venom glands, but also have toxic components in other parts of the adult spiders, and even in the newborn spiderlings and unhatched eggs. The venom and venom toxins secreted by their venom glands have been quite extensively studied and, comparatively, the study on the toxins outside venom glands is limited. Although the toxins outside venom glands were discovered at a very early time, it is not until recently that the molecular basis and mechanism of the toxicity outside venom glands have been relatively systematically investigated, which have significantly expanded our understanding of the spider toxins. This review summarizes the progresses in research on <em>Latrodectus</em> spp., particularly black widow spider, toxins outside venom glands, with an emphasis on toxins from the spider eggs.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"264 ","pages":"Article 108437"},"PeriodicalIF":2.6,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144209626","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}

{"title":"The natural compounds derived from the plant Moquiniastrum polymorphum subsp. polymorphum prevent and treat liver fibrosis in vivo by reducing inflammation and fibrotic markers","authors":"Matheus Scherer Bastos ,&nbsp;Kétlin Fernanda Rodrigues ,&nbsp;Maria Claudia Rosa Garcia ,&nbsp;Carolina Luft ,&nbsp;Giovana Vivan Tonial ,&nbsp;Giovanna Mezzomo Pavanato ,&nbsp;Leandro Vieira Astarita ,&nbsp;Barbara Bettanin Gatti ,&nbsp;Fábio Luiz Dal Moro Maito ,&nbsp;Eliane Romanato Santarém ,&nbsp;J.R. de Oliveira","doi":"10.1016/j.toxicon.2025.108436","DOIUrl":"10.1016/j.toxicon.2025.108436","url":null,"abstract":"<div><div>Natural compounds, such as extracts and coumaric acid from <em>Moquiniastrum polymorphum</em> subsp. <em>polymorphum</em> (MP), have shown promise as alternatives for treating inflammatory and oxidative diseases, including liver fibrosis, by reversing hepatic stellate cell activation in vitro. This study aimed to evaluate the treatment and prevention potential of MP and coumaric acid in an in vivo model of liver fibrosis. BALB/c mice were subjected to liver fibrosis induction via carbon tetrachloride (CCl4), followed by treatment with MP extracts and coumaric acid. The compounds present in the extracts were quantified using GCMS analysis. The results demonstrated that MP and coumaric acid reduced liver damage by decreasing serum enzyme levels, attenuating oxidative stress, and diminishing inflammation and fibrosis. This was supported by reduced mRNA expression of fibrotic genes such as α-SMA and Col-1, alongside inhibition of the NF-kB-mediated inflammatory pathway. These findings highlight the potential of MP extracts and coumaric acid for managing CCl4-induced liver fibrosis. Future studies are essential to isolate and characterize the active compounds, ensuring their efficacy and safety as therapeutic agents for chronic liver diseases.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"264 ","pages":"Article 108436"},"PeriodicalIF":2.6,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144195393","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}

{"title":"Nutrient regulation targeting macrophage-controlled intestinal mucosal healing: A promising strategy against intestinal mucositis induced by deoxynivalenol","authors":"Simin Wu ,&nbsp;Xinyu Fang ,&nbsp;Jinfeng Zhao ,&nbsp;Gang Liu ,&nbsp;Peng Liao","doi":"10.1016/j.toxicon.2025.108434","DOIUrl":"10.1016/j.toxicon.2025.108434","url":null,"abstract":"<div><div>Deoxynivalenol (DON), one of the most severely polluting mycotoxins globally, contaminates agricultural products and food through environmental pathways, compromising intestinal barrier integrity and homeostasis in humans and animals. This disruption triggers intestinal mucositis and exacerbates inflammatory bowel disease (IBD) progression. Current therapies focusing on immunosuppression face limitations due to drug resistance, shifting research toward mucosal healing strategies for sustained remission. Macrophages, essential mediators of intestinal immunity, exhibit metabolic and phenotypic plasticity critical for mucosal repair. Emerging evidence highlights nutrient-mediated metabolic reprogramming as a potential approach to enhance macrophage-driven mucosal healing and barrier restoration. This review synthesizes DON-induced intestinal toxicity mechanisms, discusses the complex functions of macrophages in intestinal mucosal healing, and highlights the current advances of nutrients regulation targeting macrophages to promote intestinal mucosal healing. Finally, feasible research directions for mitigating DON-related health risks through innovative nutritional strategies are proposed, emphasizing translational applications in food safety and precision nutrition.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"264 ","pages":"Article 108434"},"PeriodicalIF":2.6,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144195392","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}

{"title":"Corrigendum to ‘Occurrence of regulated, emerging, and masked mycotoxins in Chinese wheat between 2021 and 2022’ [Toxicon 260 (2025) 108344]","authors":"Yujing Luan ,&nbsp;Dawei Zhang ,&nbsp;Zhinan Liu ,&nbsp;Xiaoyu Sun ,&nbsp;Xuetao Yang","doi":"10.1016/j.toxicon.2025.108435","DOIUrl":"10.1016/j.toxicon.2025.108435","url":null,"abstract":"","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"263 ","pages":"Article 108435"},"PeriodicalIF":2.6,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167996","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}

{"title":"Ezetimibe protects against alpha-amanitin-induced hepatotoxicity by targeting the NTCP receptor: Mechanistic insights from in vitro and in vivo models","authors":"Jinfang Xue ,&nbsp;Xiran Lou ,&nbsp;Deyuan Ning ,&nbsp;Yan Yang ,&nbsp;Ruifei Shao ,&nbsp;Yu Liu ,&nbsp;Zhuange Shi ,&nbsp;Ruanxian Dai ,&nbsp;Fuping Wang ,&nbsp;Guobing Chen","doi":"10.1016/j.toxicon.2025.108423","DOIUrl":"10.1016/j.toxicon.2025.108423","url":null,"abstract":"<div><h3>Background</h3><div>α-Amanitin, the primary lethal toxin of <em>Amanita phalloides</em>, induces irreversible hepatotoxicity by selectively inhibiting RNA polymerase II, leading to transcriptional arrest. Despite advancements in managing mushroom poisoning, a targeted antidote remains unavailable. The sodium taurocholate co-transporting polypeptide (NTCP), a hepatic bile acid transporter, facilitates α-amanitin entry into hepatocytes. Pharmacological blockade of NTCP represents a promising therapeutic strategy.</div></div><div><h3>Objective</h3><div>To evaluate ezetimibe, an NTCP inhibitor, as a protective agent against α-amanitin-induced hepatotoxicity.</div></div><div><h3>Methods</h3><div>Transcriptomic profiling of α-amanitin-exposed mouse liver tissues (NCBI accession: PRJNA809431) was conducted using DESeq2. Molecular docking simulations assessed interactions between NTCP, α-amanitin, and ezetimibe. Therapeutic efficacy was evaluated in vivo (mouse models) and in vitro (cultured hepatocytes). Key outcomes included survival rates, liver injury markers (ALT, AST), apoptosis (Bax/Bcl-2 ratio), and oxidative stress parameters.</div></div><div><h3>Results</h3><div>NTCP expression was upregulated in α-amanitin-exposed livers. Molecular docking revealed α-amanitin binding at NTCP residue VAL-160, whereas ezetimibe interacted with LEU-14 and ASN-17. Ezetimibe (50 mg/kg) improved survival rates from 25 % to 80 % in α-amanitin-exposed mouse models (<em>p</em> &lt; 0.01), reduced serum ALT (68 ± 5 U/L vs. 165 ± 12 U/L; <em>p</em> &lt; 0.05) and AST (72 ± 6 U/L vs. 158 ± 10 U/L; <em>p</em> &lt; 0.05), and attenuated apoptosis (60 % decrease in Bax/Bcl-2; <em>p</em> &lt; 0.05). In vitro, ezetimibe restored hepatocyte viability 2.1-fold (<em>p</em> &lt; 0.05) and reduced oxidative stress (40 % decrease in malondialdehyde; <em>p</em> &lt; 0.05). Transcriptomic analysis linked α-amanitin toxicity to <em>p53</em>-mediated apoptosis.</div></div><div><h3>Conclusion</h3><div>Ezetimibe protects against α-amanitin hepatotoxicity by blocking NTCP-mediated uptake, supporting its potential clinical repurposing as a targeted antidote.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"264 ","pages":"Article 108423"},"PeriodicalIF":2.6,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144192287","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}

{"title":"The interaction of HT-2 toxin and Akt1 on gene expression regulation in Kashin-Beck disease pathogenesis","authors":"Xinhua Liao ,&nbsp;Xiaodong Yang ,&nbsp;Xiaoqian Jia ,&nbsp;Qian Zhang ,&nbsp;Gaowa Naren ,&nbsp;Jiaojiao Zhang ,&nbsp;Hui Niu ,&nbsp;Haiyan Wei ,&nbsp;Cuiyan Wu","doi":"10.1016/j.toxicon.2025.108432","DOIUrl":"10.1016/j.toxicon.2025.108432","url":null,"abstract":"<div><h3>Background</h3><div>This study investigates the effects of T-2 toxin metabolite HT-2 alone or combined with Akt1 on chondrocyte gene expression to elucidate their roles in Kashin-Beck disease (KBD) pathogenesis.</div></div><div><h3>Methods</h3><div>Lentiviral transfection was employed to silence <em>Akt1</em> in C28/I2 human chondrocytes. High-throughput RNA sequencing and bioinformatics analysis methods were used to identify and compare differentially expressed genes (DEGs) and pathways in HT-2, si<em>Akt1</em>, HT-2-si<em>Akt1</em> and Control (non-treatment) group. Co-expressed genes and co-expressed modules were investigated using WGCNA. Protein-protein interaction (PPI) networks were constructed using the STRING database, and hub genes were identified by the MCC algorithm.</div></div><div><h3>Results</h3><div>A total of 2086 DEGs were identified in the HT-2 vs Control comparison, with significant upregulation observed for CCND2, MMP9 and TIMP4. The adhesion and PI3K-<em>Akt</em> signaling pathways were upregulated, while ECM-receptor interactions was downregulated. In the siAkt1 vs Control comparison, 695 DEGs were detected. VAMP7 and CXCR4 were significantly upregulated, while PFKL and ALDOA were significantly downregulated. Fructose and mannose metabolism, amino acid biosynthesis, and glucose/energy metabolic pathways were significantly downregulated. There were 411 DEGs when HT-2-si<em>Akt1</em> vs HT-2, and CCND2, MMP9, WTAPP1 and TIMP4 were significantly downregulated. Adhesion, NF-κB signaling pathway and PI3K-<em>Akt</em> signaling pathway were significantly downregulated. Under, WGCNA, in the module most associated with HT-2, FRMD3B, ALDH1A3, ANTXR2, SERINC2 and SRGN were identified as hub genes; in the module most associated with si<em>Akt1</em>, TNFRSF11B, CECR2, TMOD1, ZNF704 and RHOBTB1 were identified as hub genes; in the module most associated with HT-2-si<em>Akt1</em>, the hub genes were GNAL, SLC25A32, ACADSB, CABLES1 and GINS4.</div></div><div><h3>Conclusion</h3><div><em>Akt1</em> primarily affects the expression of genes in chondrocytes under HT-2 exposure that involved in autophagy, cell proliferation and glycolysis and other cell functions, potentially contributing to the pathogenesis of KBD.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"264 ","pages":"Article 108432"},"PeriodicalIF":2.6,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144192288","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}

{"title":"Exploring the cytotoxicity of phytochemicals: Comparative analysis of single and combination therapies in multiple cell lines","authors":"Fatemeh Haghani ,&nbsp;Sorour Ashaari ,&nbsp;Narges Ashraf Ganjooei ,&nbsp;Behzad Behnam ,&nbsp;Prashant Kesharwani ,&nbsp;Amirhossein Sahebkar","doi":"10.1016/j.toxicon.2025.108433","DOIUrl":"10.1016/j.toxicon.2025.108433","url":null,"abstract":"<div><div>We aimed to determine and compare the cytotoxic effects of curcumin (Cur), gingerol (Gin), berberine (Ber), resveratrol (Res), baicalin (Bai), and epigallocatechin-3-gallate (EGCG) both individually and in combination, across MCF-7, 3T3, A549, PC-12, and HT-29 cell lines. The findings also showed that IC50 values were not achieved for Bai and EGCG in all exposed cell lines. Furthermore, Cur was the most potent cytotoxic agent in monotherapy. In combination therapy, the Cur + Res combination indicated the most inhibitory effect in MCF-7 cells. The most inhibitory effects were for Res + Bai and Cur + Res combinations in 3T3 cells. In the resistant A549 cells, the combined administration of phytochemical enhanced cytotoxic effects. The combinations of Cur + Gin, Cur + Res, and Cur + Ber were identified as the most effective inhibitors in the PC-12 cell line. In HT-29 cells, the combinations of Cur + Gin, Cur + Res, Cur + Ber, and Cur + Res + Gin exhibited the highest inhibitory effects. Based on these findings, Cur was the most cytotoxic agent in monotherapy, while Cur + Res exhibited the greatest cytotoxicity in combination therapy. Moreover, combination therapy led to increased cytotoxic actions of phytochemicals in resistant cells. Therefore, combinational administration is recommended for future anti-cancer studies, as it allows for the use of lower concentrations of each phytochemical.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"263 ","pages":"Article 108433"},"PeriodicalIF":2.6,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144185129","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}

{"title":"Oral Bee Venom as a Novel Therapeutic Approach for Diabetic Nephropathy in Rats: Role of PI3K, AMPK, and VEGF Signaling","authors":"Amany N. Ahmed ,&nbsp;Dina H. Merzeban ,&nbsp;Doaa E. Eldosoki Mohammed ,&nbsp;Rania H. Mahmoud ,&nbsp;Amr A.A. Metwally ,&nbsp;Sayed M. Metwally Mizar","doi":"10.1016/j.toxicon.2025.108422","DOIUrl":"10.1016/j.toxicon.2025.108422","url":null,"abstract":"<div><div>Diabetic nephropathy is a significant global health concern. While bee venom has shown potential in treating diabetes mellitus, its efficacy in managing diabetic nephropathy remains unclear. Moreover, the painful nature of bee venom injections besides its possible allergic reaction limits its widespread use. Thus, this study investigates the possible efficacy of oral bee venom administration compared to subcutaneous injection in treating diabetic nephropathy, focusing on the pathophysiological mechanisms involved. Thirty two rats were divided into four groups: normal control, diabetic control, subcutaneous bee venom (0.5 mg/kg daily), and oral bee venom (1 mg/kg in drinking water daily). Diabetes was induced in obese male albino rats using streptozotocin, followed by four weeks bee venom treatment. The present results revealed that the increased fasting glucose, insulin levels, HOMA-IR and serum creatinine in the diabetic control group, were restored to near-normal values with both bee venom-administration routes. Pi3K and AMPK, and the autophagy marker, Beclin-1, were downregulated in diabetic controls. Both bee venom treatments upregulated these genes. Additionally, immunohistochemistry revealed increased eNOS and VEGF in diabetic controls that decreased with both bee venom treatments. In conclusion. Oral bee venom effectively ameliorates diabetic nephropathy in rats through the upregulation of Pi3K, AMPK, Beclin-1, and decreased eNOS, and VEGF immunohistochemistry. Suggesting potential therapeutic applications for oral bee venom in managing diabetic nephropathy, offering a less painful and less allergic alternative to traditional subcutaneous administration.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"263 ","pages":"Article 108422"},"PeriodicalIF":2.6,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151750","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}

{"title":"Potential inhibitors of metalloproteinases (MMPs) and phospholipases from Nemopilema nomurai jellyfish peptides: An in-silico pharmacokinetics and molecular docking studies","authors":"Blessing Danso ,&nbsp;Yang Fengling ,&nbsp;Xiaoyu Hua ,&nbsp;Jinyu Zhang ,&nbsp;Jingbo Chen ,&nbsp;Yuan Yao ,&nbsp;Marina Pozzolini ,&nbsp;Fei Wang ,&nbsp;Liang Xiao ,&nbsp;Huang Ruixue","doi":"10.1016/j.toxicon.2025.108421","DOIUrl":"10.1016/j.toxicon.2025.108421","url":null,"abstract":"<div><div>Jellyfish stings, especially from <em>Nemopilema nomurai</em>, pose serious health risks due to its venom toxins like metalloproteinases (MMPs) and phospholipases A2 (PLAs A2). Thes toxin can induce severe reactions such as pain, tissue necrosis, inflammation, and in extreme cases, cardiac arrest. While the exact mechanisms of toxicity are not fully understood, MMPs and PLA2 enzymes are known to contribute significantly to tissue damage and inflammation. Thus, the inhibition of these toxins could reduce venom toxicity and provide new treatment options for jellyfish envenomation. This study utilized pharma informatic to evaluate <em>Nemopilema nomurai</em> jellyfish-derived peptides against <em>Nemopilema nomurai</em> venom toxins (metalloproteinase and phospholipase). After profiling absorption, distribution, metabolism, excretion, and toxicity (ADMET) parameters, two peptides, DN26779_N and DN26779_Q, were selected for docking analysis. DN26779_N exhibited higher binding energy to metalloproteinase (−13.3), and phospholipase (−12.6) than DN26779_Q. Molecular dynamics simulations confirmed the stability of these interactions, driven by hydrophobic affinity and hydrogen bonding. Overall, DN26779_N and DN26779_Q demonstrate significant potential as inhibitors of metalloproteinase, and phospholipase A2, presenting promising therapeutic avenues for treating and addressing jellyfish envenomation.</div></div>","PeriodicalId":23289,"journal":{"name":"Toxicon","volume":"263 ","pages":"Article 108421"},"PeriodicalIF":2.6,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143604","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}