Toxicology Research最新文献

{"title":"Exploring the causal relationship and molecular mechanisms between Methyl-4-hydroxybenzoic acid (MEP) and Alzheimer's disease: a mendelian randomization, multi-omics, and network toxicology approach.","authors":"Hong Gong, Jiayu Li, Rong Pu, Jian Huang","doi":"10.1093/toxres/tfaf113","DOIUrl":"10.1093/toxres/tfaf113","url":null,"abstract":"<p><p>The pathogenesis of Alzheimer's disease remains incompletely understood. Methyl-4-hydroxybenzoic acid, a common chemical additive, may play a role, though its mechanisms are unclear. This research investigated the potential causal link between Methyl-4-hydroxybenzoic acid and Alzheimer's disease and examined underlying molecular mechanisms. Mendelian randomization analysis evaluated causality, using Cochran's Q test, the Mendelian Randomization-Egger intercept test, and Mendelian Randomization Pleiotropy RESidual Sum and Outlier to assess heterogeneity and sensitivity. Methyl-4-hydroxybenzoic acid targets were identified through multiple databases, and a related target library was constructed using Weighted Gene Co-expression Network Analysis, differential gene expression analysis, and the Genecards database. A Protein-Protein Interaction network identified core genes, validated by molecular docking. Transcriptomic analysis and single-cell expression data explored cell-type-specific expression patterns. Results showed a significant positive causal association between Methyl-4-hydroxybenzoic acid and Alzheimer's disease. We identified 198 Methyl-4-hydroxybenzoic acid targets, with 99 genes associated with both Methyl-4-hydroxybenzoic acid and Alzheimer's disease. Six core genes (EGFR, ESR1, MAPK3, MMP9, PTGS2, TP53) were pinpointed. Functional enrichment implicated neuronal signaling, inflammation, and metabolism. Multi-omics and single-cell analyses revealed differential expression of core genes in key brain regions. Molecular docking confirmed stable interactions between Methyl-4-hydroxybenzoic acid and these proteins. This research confirms a causal relationship between Methyl-4-hydroxybenzoic acid and Alzheimer's disease, revealing potential molecular mechanisms and core gene functions, offering insights into pathogenesis and therapeutic targets.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf113"},"PeriodicalIF":2.1,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144833430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of senescence on the sensitization potential of chemicals detected by local lymph node assays in aged mice.","authors":"Koji Ishida, Mao Kaneki, Chiharu Ohira, Mana Ichikawa, Ibuki Yasuda, Chizuki Usui, Yoshiichi Takagi, Tomoki Fukuyama","doi":"10.1093/toxres/tfaf110","DOIUrl":"10.1093/toxres/tfaf110","url":null,"abstract":"<p><p>The global population is aging rapidly, posing new challenges for the safety evaluation of chemicals. Most toxicity studies use suitably aged animals that resemble healthy adults if they have similar responses. However, this assumption may not be valid because aging affects various physiological functions, such as immunity. The objective of this study was to compare the skin sensitization potential of chemicals in healthy adult mice, aged mice, and an aging mouse model using local lymph node assays (LLNA). Initially, eight-week-old female CBA/Ca, C3H/He (historical control for SAMP1 mice), senescence-accelerated mouse prone 1 (SAMP1), and C57BL6/N mice were compared to verify any differences among these strains. Next, 20-wk-old C3H/He and SAMP1 mice were compared with 80-wk-old C57BL6/N mice. Several concentrations (2.76, 8.3, and 25%) of α-hexyl cinnamaldehyde (HCA) were used as a positive substance for LLNA to determine the skin sensitization potential in each strain. The proliferation of T and B cells and related cytokine production were also measured. A dose-dependent correlation was observed, and a threshold of 1.8 for positive criteria for skin sensitization in LLNA, was surpassed in the CBA/Ca, C3H/He, and C57BL6/N strains, but not in the SAMP1 strain. In 20-wk-old mice, a positive response was observed only in C3H/He mice, whereas no positive response was observed in aged C57BL6 mice and SAMP1 mice. Our findings imply that senescence affects the skin sensitization potential of chemicals as measured using LLNA.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf110"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Albiflorin improves diabetic retinopathy by mitigating oxidative stress and inflammation via the TLR-4/NF-kB signaling pathway.","authors":"Liuyi Xie, Yingjun Wang, Yudan Gong","doi":"10.1093/toxres/tfaf105","DOIUrl":"10.1093/toxres/tfaf105","url":null,"abstract":"<p><p>This study was to investigate the effects of Albiflorin (ALB) on oxidative stress and inflammation in diabetic retinopathy (DR) and explore its potential mechanism involving the Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway. Human retinal microvascular endothelial cells (HRMECs) were treated with high glucose (HG) and ALB. Cell viability was assessed by MTT assay. Oxidative stress markers and inflammatory cytokines were measured by ELISA. TLR4/NF-κB pathway proteins were analyzed by Western blot. A streptozotocin (STZ)-induced diabetic rat model was established to examine retinal histological changes. Serum metabolic parameters, oxidative stress markers, and inflammatory cytokines were evaluated in the DR model and ALB intervention groups. Results showed that ALB improved HRMEC viability under HG induction and reduced oxidative stress and inflammation. ALB inhibited the TLR4/NF-κB pathway in HG-induced HRMECs. Overexpression of TLR4 partially reversed the protective effects of ALB. In diabetic rats, ALB ameliorated metabolic disorders, improved retinal histological structure, and reduced oxidative stress and inflammation. ALB also suppressed the TLR4/NF-κB signaling pathway <i>in vivo</i>. In conclusion, ALB improves DR by resolving oxidative stress and inflammation through inhibiting the TLR4/NF-κB signaling pathway. These findings suggest ALB as a potential therapeutic agent for DR.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf105"},"PeriodicalIF":2.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanisms of non-pharmaceutical chemicals exposure-induced liver injury: a network toxicology approach.","authors":"Tao Chen, Xing Qian, Zhi Wu","doi":"10.1093/toxres/tfaf096","DOIUrl":"10.1093/toxres/tfaf096","url":null,"abstract":"<p><p>The exposure to non-pharmaceutical chemicals has been increasingly associated with liver injury, yet the underlying molecular mechanisms remain unclear. This study investigates the impact of three such chemicals-sunset yellow (SUN), tartrazine (TART), and triclosan (TRI)-on human HepaRG cells to elucidate potential toxicological targets and pathways. We conducted differential expression analysis on HepaRG cells exposed to SUN, TART, and TRI, identifying differentially expressed genes (DEGs). Intersection analyses were performed to uncover common targets, followed by heatmap visualization and enrichment analyses using GO and KEGG pathways. Protein-protein interaction (PPI) and immune cell infiltration analyses further elaborated the effects, complemented by molecular docking studies to assess chemical binding affinities. Our findings identified 47 upregulated and 123 downregulated DEGs as common targets across all chemical exposures. Enrichment analysis revealed significant alterations in biological processes related to liver metabolism and development. Four core toxic targets (KNG1, PLG, SERPINE1, SERPINF2) were identified with significant connectivity in PPI analysis, confirmed by altered gene expression. Immune cell infiltration analysis indicated modulation of various immune cell populations. The molecular docking study highlighted strong binding of TART and SUN to PLG, suggesting a potential mechanism of liver injury. This study provides insights into the molecular mechanisms of liver injury induced by non-pharmaceutical chemical exposure, identifying key toxicological targets and pathways. The results suggest that chemicals like SUN and TART can significantly alter liver function through specific gene expression changes and immune modulation, offering potential biomarkers and therapeutic targets for mitigating such toxic effects.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf096"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effect of L-carnitine on cadmium induced neurotoxicity in rats.","authors":"Yan Wang, Yuan Hu, Chunxia Guo, Yuanjing Ma, Qizhong Qin","doi":"10.1093/toxres/tfaf111","DOIUrl":"10.1093/toxres/tfaf111","url":null,"abstract":"<p><p>Cadmium (Cd), a well-known environmental pollutant, widely exists in water, soils, sediments, and air, and produces various system dysfunctions including those affecting the nervous system. L-carnitine (L-CAR) is an antioxidant that plays neuroprotective roles by improving enzyme functions. The purpose of our study was to evaluate whether L-CAR could efficiently protest against neurotoxicity induced by Cd. Rats were exposed to different concentrations of Cd (0, 25, 50, 100 mg/l) for 4 weeks. We used the open-field test (OFT) and forced-swimming test (FST) to observe the rats'spontaneous locomotor activity and exploration behavior; brain histopathological section to observe the damage of cortical neurons in the brain; Oxidative stress indicators reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) were determined at terminal time-points. The protective effects of L-CAR(1.5 g/l) were evaluated in parallel. Here, we corroborated that that L-CAR is a potential pharmacological agent that protests against the neurotoxicity of Cd. The results of brain histopathological sections show that with the increase of cadmium dosage in drinking water, but the damage to cortical neurons becomes more severe;the Cd(100 mg/l) + L-CAR(1.5 g/l) group, the neuronal cell membrane was intact, the cell outline was clear. The Cd-induced oxidative stress in the cerebral cortex was proven by elevation of ROS, MDA levels, and reduction of SOD activity. However, those effects on oxidative stress were attenuated if L-CAR(1.5 g/l) was simultaneously administrated. The results suggested that L-CAR is a potential pharmacological agent that protects the neurotoxicity of Cd.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf111"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Puerarin alleviates high glucose-induced lens epithelial cell damage by activating the Nrf2 Signaling pathway to inhibit oxidative stress.","authors":"Juan Xia, Mingli Zhou, Yuandong Ma, Song Zhang, Shanshan Tang, Jie Zhang","doi":"10.1093/toxres/tfaf109","DOIUrl":"10.1093/toxres/tfaf109","url":null,"abstract":"<p><p>This study investigated Puerarin's protective effects and mechanisms against high glucose (HG)-induced damage in human lens epithelial cells (HLECs), which are relevant to diabetic complications. Using an HG-exposed HLEC model, varying doses of Puerarin (10 μM, 20 μM, 50 μM) were tested. While non-toxic to normal HLECs, both 20 μM and 50 μM Puerarin significantly and dose-dependently restored cell viability reduced by HG (<i>P</i> < 0.05). Puerarin effectively reversed HG-induced apoptosis and mitigated oxidative stress by increasing levels of antioxidant enzymes (SOD, GSH-Px) and decreasing malondialdehyde (MDA) concentrations. Mechanistically, Puerarin significantly upregulated the expression of the transcription factor Nrf2, with the strongest effect observed at 50 μM. Crucially, when Nrf2 expression was knocked down using shRNA Nrf2 transfection in HG-treated HLECs, the protective effects of high-dose Puerarin were completely abolished. This loss of protection resulted in significantly increased cell death and oxidative stress markers compared to control cells transfected with shRNA Ctrl and treated with Puerarin. The findings demonstrate that Puerarin, particularly at doses of 20 μM and 50 μM, protects HLECs from HG-induced damage in a dose-dependent manner. This protection involves preserving cell viability, reducing apoptosis, and enhancing cellular antioxidant defenses. The Nrf2 signaling pathway is identified as a key mechanism mediating Puerarin's beneficial effects. These results suggest that Puerarin has potential as a therapeutic agent for preventing diabetic complications affecting the lens epithelium.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf109"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nitrate protects against methotrexate-induced liver injury by activating Wnt/β-catenin Signaling in mice.","authors":"Xin Wen, Ying Liu, Chunmei Zhang, Jinsong Wang, Guangyong Sun, Dong Zhang, Songlin Wang, Shaorong Li","doi":"10.1093/toxres/tfaf107","DOIUrl":"10.1093/toxres/tfaf107","url":null,"abstract":"<p><p>Methotrexate (MTX) is a drug used to treat autoimmune diseases and certain cancers. However, its untreatable hepatotoxic effect severely limits its clinical use. Therefore, further studies are required to combat MTX-induced liver injury. Nitrate, abundant in green vegetables, possesses anti-inflammatory, antioxidant, and immunoregulatory effects. Our study investigated the preventive effects of nitrate on MTX-induced liver injury. Liver injury in mice was induced by administering a single dose of MTX (20 mg/kg body weight) intraperitoneally (i.p.). Pre-treatment of mice with 2 mM nitrate in drinking water 5 days prior effectively mitigated the MTX-elevated serum aminotransferase activities, attenuated hepatic pathological injury, reduced hepatic apoptosis and restored the proliferative capacity of hepatocytes. RNA sequencing analysis indicated that the molecular mechanism may involve the activation of the Wnt/β-catenin pathway. The AML 12 cell line was employed for <i>in vitro</i> validation. In this study, the hepatoprotective effect of nitrate against drug-induced liver injury (DILI) was identified for the first time, providing a new approach to preventing DILI in clinical practice.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf107"},"PeriodicalIF":2.1,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144751907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Accuracy of Pediatric new poisoning mortality score versus poisoning severity score in prediction of in-hospital mortality of acutely poisoned children admitted to Pediatric intensive care unit.","authors":"Meray Medhat Shokry Zaghary, Hend Gamal Aref, Wafaa Abdel-Ghaffar Ali","doi":"10.1093/toxres/tfaf108","DOIUrl":"10.1093/toxres/tfaf108","url":null,"abstract":"<p><p>Acute pediatric poisoning is a severe global public health issue that represents a leading cause of morbidity and mortality in pediatrics. The study discussed the accuracy rate of the new PMS to be applied to pediatric acutely poisoned patients after modification to be called the pediatric new poisoning mortality score (pediatric new-PMS) and compared it to the poisoning severity score (PSS). The study was conducted on acutely pediatric intoxicated patients admitted to a pediatric intensive care unit (PICU) during the period from January 2021 to January 2024 (181 cases). 48.6% of cases were males, and 51.4% were females; the median age was 5 years. Regarding the fate of cases, 65.2% recovered completely, 16.57% recovered with a complicated course, and 18.23% died. The pediatric new-PMS above 50 points had an accuracy rate of 85.3% with good discrimination for mortality, sensitivity of 78.8%, specificity of 77.7%, positive predictive value of 44%, and negative predictive value of 94%. The PSS above 2 had an accuracy rate of 84.5% with good discrimination for mortality, sensitivity of 97%, specificity of 71.6%, positive predictive value of 43.2%, and negative predictive value of 99%. The study concluded that the PSS and pediatric new PMS can be used efficiently to predict mortality in acute pediatric intoxicated patients. The pediatric new-PMS score is easy to calculate even before admission to PICU, as it depends on objective markers that can be obtained even in the prehospital stage, such as vital signs, mental state, demographics, and poisoning-related variables.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf108"},"PeriodicalIF":2.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144758740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zearalenone induces GnRH neurons activation related to central precocious puberty by triggering MKRN3 auto-ubiquitination and down-regulation.","authors":"Yan Sun","doi":"10.1093/toxres/tfaf106","DOIUrl":"10.1093/toxres/tfaf106","url":null,"abstract":"<p><p>Central precocious puberty (CPP) refers to gonadotropin-dependent sexual precocity that results from the early activation of the hypothalamic-pituitary-gonadal (HPG) axis. Zearalenone (ZEA), a non-steroidal mycotoxin, is one of the important triggering factors for the development of CPP; however, its regulatory mechanism remains unclear. In this study, the correlation between urinary zearalenone (ZEA) levels and the blood expression of MKRN3 (makorin RING-finger protein-3) in patients with central precocious puberty (CPP) was investigated. Subsequently, the regulatory mechanism of ZEA on MKRN3, as well as its association with gonadotropin-releasing hormone (GnRH) production, cell proliferation, and the expression and localization of the G protein-coupled estrogen receptor (GPER) were explored in the hypothalamic cell line GT1-7. Analysis of clinical samples revealed that urinary ZEA levels were negatively correlated with blood MKRN3 expression in CPP patients. The in vitro experiments revealed that ZEA treatment up-regulated cell proliferation as well as the expressions of GnRH and GPER and re-location of GPER in GT1-7 cells by triggering MKRN3 auto-ubiquitination and down-regulation. However, such effects were attenuated by GPER overexpression. In conclusion, this study reveals a novel mechanism by which ZEA influences CPP using clinical samples and an in vitro model. The findings suggest that MKRN3 may serve as a potential therapeutic target and a diagnostic biomarker for CPP.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf106"},"PeriodicalIF":2.9,"publicationDate":"2025-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of an epitope-based vaccine from <i>mycoplasma genitalium</i> adhesion protein: addressing antibiotic resistance through immune-informatics.","authors":"Hafiz Muhammad Rehman, Muhammad Bilal, Muhammad Shoaib, Tahir Latif, Rabbani Syed, Fahid Khalid, Muhammad Naveed Khan, Saira Asif Khan, Nadeem Ahmed, Saad Tahir, Hamid Bashir","doi":"10.1093/toxres/tfaf102","DOIUrl":"10.1093/toxres/tfaf102","url":null,"abstract":"<p><p><i>Mycoplasma genitalium</i> is increasingly recognized for its role in severe health conditions, including sexually transmitted infections, ovarian and prostate cancer. The adhesion protein plays a crucial role in the pathogen's ability to attach to and invade host cells, making it a key target for vaccine development. The need to develop a vaccine against <i>M. genitalium</i> stems from its rising antibiotic resistance, limited treatments and effectiveness. This study focuses on the design and computational evaluation of adhesion protein-based epitope vaccine. Through an immunoinformatic approach, multiple novel cytotoxic T lymphocyte (CTL), helper T lymphocyte (HTL), and linear B-cell epitopes were identified from the adhesion protein, demonstrating strong antigenic, non-allergenic, and immunogenic properties. The vaccine construct's 3D structure was validated using Ramachandran plot analysis, ProSA, and ERRAT servers, confirming its stability and suitability. Molecular docking studies revealed a high binding affinity of the vaccine with the TLR-2 receptor, further supported by 100 ns molecular dynamics (MD) simulations that confirmed the structural stability and robust interaction of the vaccine with immune receptors. In silico immune simulations using the C-ImmSim server demonstrated the vaccine's potential to elicit strong humoral and cell-mediated immune responses. Codon optimization for expression in <i>E. coli</i> using the pET-29a(+) vector predicted efficient production of the vaccine. The comprehensive computational analysis, underscores the potential of this epitope-based vaccine as a promising candidate against <i>M. genitalium</i> infections. However, the study emphasizes the necessity of in vitro and in vivo experiments to validate the vaccine's efficacy and safety before advancing to clinical trials.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf102"},"PeriodicalIF":2.9,"publicationDate":"2025-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}