Pub Date : 2026-01-21DOI: 10.1016/j.abst.2026.01.007
Muhammad Waqas , Hafiz Muhammad Javed , Muhammad Faisal Khan , Iqra Batool , Tehmina Saddique , Khadija Munir , Razia Bashir
Diabetes mellitus remains a major global health challenge, affecting over 537 million adults worldwide and this number is expected to rise 783 million by 2045, underscoring the need for improved therapeutic strategies. In this study, we synthesized and evaluated ellagic-acid-loaded gold nanoparticles (EA-AuNPs) prepared from Syzygium cumini seed extract as a potential antidiabetic intervention. EA-AuNPs exhibited a spherical morphology with an average size of 68.4 ± 5.2 nm, zeta potential of −24.6 mV, and encapsulation efficiency of 81.3 ± 2.7 %, indicating stability and optimal drug-loading capacity. In vivo testing in streptozotocin-induced diabetic mice (n = 40) revealed that EA-AuNPs (25 mg/kg, orally, for 28 days) reduced fasting blood glucose by 68.3 % (p < 0.001) and HbA1c by 43.5 % (p < 0.01), while enhancing serum insulin by 2.8-fold. Histological assessment showed restoration of islet morphology with an increase in β-cell area, consistent with protective and recovery-associated effects. Multi-omics analyses supported modulation of metabolic and inflammatory pathways, including PI3K/AKT, AMPK, and NF-κB, consistent with improved glucose homeostasis and reduced oxidative stress (MDA ↓52.4 %, SOD ↑2.1-fold). Collectively, these findings suggest that EA-AuNPs may offer a promising nanophytochemical approach for managing Type 2 diabetes, warranting further mechanistic and translational investigation.
{"title":"In vivo multi-omics evaluation of ellagic Acid–Gold nanoparticles from Syzygium cumini for glycemic improvement and β-cell preservation in type 2 diabetic mice","authors":"Muhammad Waqas , Hafiz Muhammad Javed , Muhammad Faisal Khan , Iqra Batool , Tehmina Saddique , Khadija Munir , Razia Bashir","doi":"10.1016/j.abst.2026.01.007","DOIUrl":"10.1016/j.abst.2026.01.007","url":null,"abstract":"<div><div>Diabetes mellitus remains a major global health challenge, affecting over 537 million adults worldwide and this number is expected to rise 783 million by 2045, underscoring the need for improved therapeutic strategies. In this study, we synthesized and evaluated ellagic-acid-loaded gold nanoparticles (EA-AuNPs) prepared from <em>Syzygium cumini</em> seed extract as a potential antidiabetic intervention. EA-AuNPs exhibited a spherical morphology with an average size of 68.4 ± 5.2 nm, zeta potential of −24.6 mV, and encapsulation efficiency of 81.3 ± 2.7 %, indicating stability and optimal drug-loading capacity. In vivo testing in streptozotocin-induced diabetic mice (n = 40) revealed that EA-AuNPs (25 mg/kg, orally, for 28 days) reduced fasting blood glucose by 68.3 % (p < 0.001) and HbA1c by 43.5 % (p < 0.01), while enhancing serum insulin by 2.8-fold. Histological assessment showed restoration of islet morphology with an increase in β-cell area, consistent with protective and recovery-associated effects. Multi-omics analyses supported modulation of metabolic and inflammatory pathways, including PI3K/AKT, AMPK, and NF-κB, consistent with improved glucose homeostasis and reduced oxidative stress (MDA ↓52.4 %, SOD ↑2.1-fold). Collectively, these findings suggest that EA-AuNPs may offer a promising nanophytochemical approach for managing Type 2 diabetes, warranting further mechanistic and translational investigation.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 236-253"},"PeriodicalIF":0.0,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-14DOI: 10.1016/j.abst.2026.01.003
K.M. Yeaser Arafat, Ahmed Hossain, Mushfika Ikfat, Md. Areful Amin, Kazi Tanvir, Dipta Gomes, Mahfujur Rahman
Ovarian cancer remains one of the most lethal gynecological malignancies, largely due to delayed diagnosis and the absence of reliable early screening tools. This study proposes an interpretable machine learning framework that integrates Fuzzy Random Forest (FRF) with Harris Hawks Optimization (HHO) for early ovarian cancer prediction using routine clinical data. The analysis was conducted on a publicly available dataset comprising 349 patient records with 51 clinical and biochemical features. To mitigate overfitting and data leakage, Recursive Feature Elimination with Cross-Validation (RFECV), preprocessing, and SMOTE–Tomek balancing were applied exclusively within the training data. A total of 31 relevant biomarkers were selected for model development. The HHO-optimized FRF achieved an accuracy of 94.12%, precision of 91.43%, recall of 96.07%, and an F1-score of 93.69%, outperforming several baseline ensemble and gradient boosting models evaluated under identical experimental conditions. Model interpretability was enhanced through SHAP and LIME analyses, which consistently identified AFP, HE4, CA125, and Age as influential predictors, aligning with established clinical knowledge. The high recall indicates strong sensitivity to cancer cases, an essential requirement for diagnostic support. Despite encouraging performance, the study is limited by its moderate sample size and a retrospective design. Consequently, the findings should be interpreted as preliminary. Future work will focus on validation using larger, multi-center cohorts and prospective studies to assess generalizability and clinical scalability.
{"title":"FRF-HHO: Early ovarian cancer prediction using explainable fuzzy random forest optimized by Harris Hawks algorithm","authors":"K.M. Yeaser Arafat, Ahmed Hossain, Mushfika Ikfat, Md. Areful Amin, Kazi Tanvir, Dipta Gomes, Mahfujur Rahman","doi":"10.1016/j.abst.2026.01.003","DOIUrl":"10.1016/j.abst.2026.01.003","url":null,"abstract":"<div><div>Ovarian cancer remains one of the most lethal gynecological malignancies, largely due to delayed diagnosis and the absence of reliable early screening tools. This study proposes an interpretable machine learning framework that integrates Fuzzy Random Forest (FRF) with Harris Hawks Optimization (HHO) for early ovarian cancer prediction using routine clinical data. The analysis was conducted on a publicly available dataset comprising 349 patient records with 51 clinical and biochemical features. To mitigate overfitting and data leakage, Recursive Feature Elimination with Cross-Validation (RFECV), preprocessing, and SMOTE–Tomek balancing were applied exclusively within the training data. A total of 31 relevant biomarkers were selected for model development. The HHO-optimized FRF achieved an accuracy of 94.12%, precision of 91.43%, recall of 96.07%, and an F1-score of 93.69%, outperforming several baseline ensemble and gradient boosting models evaluated under identical experimental conditions. Model interpretability was enhanced through SHAP and LIME analyses, which consistently identified AFP, HE4, CA125, and Age as influential predictors, aligning with established clinical knowledge. The high recall indicates strong sensitivity to cancer cases, an essential requirement for diagnostic support. Despite encouraging performance, the study is limited by its moderate sample size and a retrospective design. Consequently, the findings should be interpreted as preliminary. Future work will focus on validation using larger, multi-center cohorts and prospective studies to assess generalizability and clinical scalability.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 219-235"},"PeriodicalIF":0.0,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-12DOI: 10.1016/j.abst.2026.01.004
Mohit , Sheetal Verma , Jyoti Bajpai
Obstructive Sleep Apnea (OSA) is a condition that obstructs the upper airway during sleep, inducing intermittent hypoxia that affects the host metabolism, and is associated with gut microbiome dysbiosis. The bidirectional link between host immunometabolism and the cardiovascular system connects with the gut microbiome and has emerged as a research interest in recent years. The gut microbiota is recognized as a potential contributor of OSA related comorbidities, including cardiovascular risk. Recent studies have demonstrated that alterations in gut microbial composition are associated with OSA and intermittent hypoxia. Remarkably, the gut-derived metabolite trimethylamine N-oxide (TMAO) has emerged as a putative metabolic link in OSA-associated cardiometabolic risk. In case of OSA, the dysregulated gut metabolic axis may elevate TMAO, which may contribute to endothelial dysfunction and cardiovascular risk. Interestingly, experimental studies suggest that hepatic flavin-containing monooxygenase 3 (FMO3), which catalyzes TMAO production, may be influenced by hypoxia-responsive metabolic pathways, raising the possibility that OSA could affect not only the gut microbiome but also host enzymatic regulation. This perspective will enhance and promote gut microbial-based sleep research, particularly targeted TMAO for the potential risk assessment and as a cardiometabolic marker in OSA. We propose that TMAO may hold potential as a cardiometabolic biomarker in OSA, warranting further validation.
{"title":"Exploring trimethylamine N-oxide (TMAO) as a metabolic link between obstructive sleep apnea and cardiovascular risk: A cardiometabolic perspective","authors":"Mohit , Sheetal Verma , Jyoti Bajpai","doi":"10.1016/j.abst.2026.01.004","DOIUrl":"10.1016/j.abst.2026.01.004","url":null,"abstract":"<div><div>Obstructive Sleep Apnea (OSA) is a condition that obstructs the upper airway during sleep, inducing intermittent hypoxia that affects the host metabolism, and is associated with gut microbiome dysbiosis. The bidirectional link between host immunometabolism and the cardiovascular system connects with the gut microbiome and has emerged as a research interest in recent years. The gut microbiota is recognized as a potential contributor of OSA related comorbidities, including cardiovascular risk. Recent studies have demonstrated that alterations in gut microbial composition are associated with OSA and intermittent hypoxia. Remarkably, the gut-derived metabolite trimethylamine N-oxide (TMAO) has emerged as a putative metabolic link in OSA-associated cardiometabolic risk. In case of OSA, the dysregulated gut metabolic axis may elevate TMAO, which may contribute to endothelial dysfunction and cardiovascular risk. Interestingly, experimental studies suggest that hepatic flavin-containing monooxygenase 3 (FMO3), which catalyzes TMAO production, may be influenced by hypoxia-responsive metabolic pathways, raising the possibility that OSA could affect not only the gut microbiome but also host enzymatic regulation. This perspective will enhance and promote gut microbial-based sleep research, particularly targeted TMAO for the potential risk assessment and as a cardiometabolic marker in OSA. We propose that TMAO may hold potential as a cardiometabolic biomarker in OSA, warranting further validation.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 208-210"},"PeriodicalIF":0.0,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic inflammation, gut microbial dysbiosis, and metabolic dysregulation are closely interrelated and play a significant role in the pathogenesis of type 2 diabetes, a long-recognized global health problem. Akkermansia muciniphila has been identified as a predominant bacterial species that plays a crucial role in maintaining gut homeostasis. This mucin-degrading gram-negative bacterium stimulates mucus production and enhances the expression of tight junction proteins, thereby maintaining intestinal barrier integrity. Moreover, it helps to prevent metabolic endotoxemia and systemic inflammation, which are the key factors contributing to the progression of type 2 diabetes and insulin resistance. This process plays a crucial role in maintaining the integrity of the intestinal barrier. Research has indicated that a higher level of A. muciniphila is associated with improved metabolic health, while a lack of it is linked to insulin resistance and obesity. Potential treatments for type 2 diabetes include probiotic therapy, polyphenol-rich diets, and prebiotic supplements that increase A. muciniphila levels. This review emphasizes the potential of A. muciniphila as a novel microbiome-directed strategy for the treatment of metabolic diseases as well as its complex role in gut health. Targeted modulation of the gut microbiota may reduce the risk of type 2 diabetes by improving intestinal barrier function, lowering metabolic endotoxemia, and suppressing chronic inflammation.
{"title":"Role of Akkermansia muciniphila in improving gut health for the prevention of type 2 diabetes","authors":"Saranyadevi Subburaj , Selva Kumar Thirumalaisamy , Jisha Jacob , Princy Vijayababu","doi":"10.1016/j.abst.2026.01.002","DOIUrl":"10.1016/j.abst.2026.01.002","url":null,"abstract":"<div><div>Chronic inflammation, gut microbial dysbiosis, and metabolic dysregulation are closely interrelated and play a significant role in the pathogenesis of type 2 diabetes, a long-recognized global health problem. <em>Akkermansia muciniphila</em> has been identified as a predominant bacterial species that plays a crucial role in maintaining gut homeostasis. This mucin-degrading gram-negative bacterium stimulates mucus production and enhances the expression of tight junction proteins, thereby maintaining intestinal barrier integrity. Moreover, it helps to prevent metabolic endotoxemia and systemic inflammation, which are the key factors contributing to the progression of type 2 diabetes and insulin resistance. This process plays a crucial role in maintaining the integrity of the intestinal barrier. Research has indicated that a higher level of <em>A. muciniphila</em> is associated with improved metabolic health, while a lack of it is linked to insulin resistance and obesity. Potential treatments for type 2 diabetes include probiotic therapy, polyphenol-rich diets, and prebiotic supplements that increase <em>A. muciniphila</em> levels. This review emphasizes the potential of <em>A. muciniphila</em> as a novel microbiome-directed strategy for the treatment of metabolic diseases as well as its complex role in gut health. Targeted modulation of the gut microbiota may reduce the risk of type 2 diabetes by improving intestinal barrier function, lowering metabolic endotoxemia, and suppressing chronic inflammation.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 211-218"},"PeriodicalIF":0.0,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-07DOI: 10.1016/j.abst.2026.01.001
David B. Ouko , Fredrick M. Musila , Peris W. Amwayi , Victoria K. Mwaeni , Dickson B. Kinyanyi , Grace W. Gitau , Alfred Orina Isaac , James Nyabuga Nyariki
Background
Plasmodium falciparum, the primary causative agent of severe malaria, catabolizes hemoglobin to obtain nutrients, resulting in the accumulation of toxic free heme. To mitigate this toxicity, the parasite converts heme into inert hemozoin. Chloroquine inhibits this detoxification process, leading to the buildup of free heme and exacerbating oxidative stress. Recent studies suggest that Coenzyme Q10 (CoQ10) may counteract malaria-induced oxidative stress and inflammation. However, its molecular interactions with key biomolecules remain unclear. This study aims to evaluate the potential molecular interactions of Coenzyme Q10 with heme and hemoglobin using an in silico approach.
Material and methods
The study involved molecular docking of Coenzyme Q10 on heme-hemoglobin, ADMET studies of Coenzyme Q10 and molecular dynamic simulations of Coenzyme Q10-heme-hemoglobin complex.
Results
Coenzyme Q10 has favorable ADMET properties and positively interacts with the heme group and some amino acids of the hemoglobin, forming a stable complex, though its ADMET profile presents challenges such as poor solubility. These findings demonstrate that Coenzyme Q10 can reduce the degradation of hemoglobin via direct interaction, subsequently regulating heme build-up.
Conclusion
This study identifies potential molecular interactions between Coenzyme Q10 and heme–hemoglobin complexes based on computational analyses, providing molecular-level insights which may infer functional or therapeutic outcomes.
{"title":"In silico analysis of Coenzyme Q10 interaction with the heme-hemoglobin complex: Implications for oxidative stress and inflammation in severe malaria","authors":"David B. Ouko , Fredrick M. Musila , Peris W. Amwayi , Victoria K. Mwaeni , Dickson B. Kinyanyi , Grace W. Gitau , Alfred Orina Isaac , James Nyabuga Nyariki","doi":"10.1016/j.abst.2026.01.001","DOIUrl":"10.1016/j.abst.2026.01.001","url":null,"abstract":"<div><h3>Background</h3><div><em>Plasmodium falciparum</em>, the primary causative agent of severe malaria, catabolizes hemoglobin to obtain nutrients, resulting in the accumulation of toxic free heme. To mitigate this toxicity, the parasite converts heme into inert hemozoin. Chloroquine inhibits this detoxification process, leading to the buildup of free heme and exacerbating oxidative stress. Recent studies suggest that Coenzyme Q10 (CoQ10) may counteract malaria-induced oxidative stress and inflammation. However, its molecular interactions with key biomolecules remain unclear. This study aims to evaluate the potential molecular interactions of Coenzyme Q10 with heme and hemoglobin using an in silico approach.</div></div><div><h3>Material and methods</h3><div>The study involved molecular docking of Coenzyme Q10 on heme-hemoglobin, ADMET studies of Coenzyme Q10 and molecular dynamic simulations of Coenzyme Q10-heme-hemoglobin complex.</div></div><div><h3>Results</h3><div>Coenzyme Q10 has favorable ADMET properties and positively interacts with the heme group and some amino acids of the hemoglobin, forming a stable complex, though its ADMET profile presents challenges such as poor solubility. These findings demonstrate that Coenzyme Q10 can reduce the degradation of hemoglobin via direct interaction, subsequently regulating heme build-up.</div></div><div><h3>Conclusion</h3><div>This study identifies potential molecular interactions between Coenzyme Q10 and heme–hemoglobin complexes based on computational analyses, providing molecular-level insights which may infer functional or therapeutic outcomes.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 199-207"},"PeriodicalIF":0.0,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-30DOI: 10.1016/j.abst.2025.12.008
Muhammad Waqas , Muhammad Umar Farooq , Tehmina Saddique , Ali Raza , Muhammad Tayyab , Razia Bashir
Type 2 diabetes mellitus remains a global health emergency, with existing therapies often failing to achieve durable glycemic control or preserve pancreatic β-cell function. In this study, we isolated and purified withacoagulin, a novel withanolide from Withania coagulans, confirmed by NMR, MS, FTIR, and HPLC (>98 % purity). A total of 72 male Wistar rats were randomized into six groups (n = 12 per group): normal control, diabetic control (streptozotocin–nicotinamide), metformin (100 mg/kg), insulin (4 U/kg), and withacoagulin at 10, and 20 mg/kg. Twelve weeks of oral withacoagulin administration resulted in significant improvements in glycemic control, including a 62 % reduction in fasting blood glucose and a 65 % decrease in HbA1c relative to diabetic controls (p < 0.001). These effects were accompanied by marked improvements in insulin sensitivity, evidenced by reduced HOMA-IR and increased QUICKI indices. Histological and immunohistochemical analyses demonstrated preservation of pancreatic islet morphology and enhanced insulin immunoreactivity in treated animals. Dyslipidemia was corrected, oxidative stress markers were improved (↑SOD, ↑CAT, ↑GPx; ↓MDA), and pro-inflammatory cytokines (TNF-α, IL-6) were significantly lowered. Mechanistic analyses demonstrated reactivation of IRS-1/PI3K/Akt signaling, increased GLUT4 translocation, and upregulation of AMPK phosphorylation, highlighting a multi-targeted mechanism of action. A 28-day subacute toxicity study conducted in accordance with OECD guidelines indicated no observable hepatic, renal, hematological, or histopathological abnormalities at doses up to 500 mg/kg, establishing a favorable preliminary safety profile. Collectively, these findings provide support for withacoagulin's potential as a mechanistically active natural lead compound for further preclinical development in metabolic disease research.
{"title":"Evaluation of withacoagulin from Withania coagulans for glycemic improvement and β-cell preservation in a type 2 diabetic model","authors":"Muhammad Waqas , Muhammad Umar Farooq , Tehmina Saddique , Ali Raza , Muhammad Tayyab , Razia Bashir","doi":"10.1016/j.abst.2025.12.008","DOIUrl":"10.1016/j.abst.2025.12.008","url":null,"abstract":"<div><div>Type 2 diabetes mellitus remains a global health emergency, with existing therapies often failing to achieve durable glycemic control or preserve pancreatic β-cell function. In this study, we isolated and purified withacoagulin, a novel withanolide from <em>Withania coagulans</em>, confirmed by NMR, MS, FTIR, and HPLC (>98 % purity). A total of 72 male Wistar rats were randomized into six groups (n = 12 per group): normal control, diabetic control (streptozotocin–nicotinamide), metformin (100 mg/kg), insulin (4 U/kg), and withacoagulin at 10, and 20 mg/kg. Twelve weeks of oral withacoagulin administration resulted in significant improvements in glycemic control, including a 62 % reduction in fasting blood glucose and a 65 % decrease in HbA1c relative to diabetic controls (p < 0.001). These effects were accompanied by marked improvements in insulin sensitivity, evidenced by reduced HOMA-IR and increased QUICKI indices. Histological and immunohistochemical analyses demonstrated preservation of pancreatic islet morphology and enhanced insulin immunoreactivity in treated animals. Dyslipidemia was corrected, oxidative stress markers were improved (↑SOD, ↑CAT, ↑GPx; ↓MDA), and pro-inflammatory cytokines (TNF-α, IL-6) were significantly lowered. Mechanistic analyses demonstrated reactivation of IRS-1/PI3K/Akt signaling, increased GLUT4 translocation, and upregulation of AMPK phosphorylation, highlighting a multi-targeted mechanism of action. A 28-day subacute toxicity study conducted in accordance with OECD guidelines indicated no observable hepatic, renal, hematological, or histopathological abnormalities at doses up to 500 mg/kg, establishing a favorable preliminary safety profile. Collectively, these findings provide support for withacoagulin's potential as a mechanistically active natural lead compound for further preclinical development in metabolic disease research.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 184-198"},"PeriodicalIF":0.0,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-29DOI: 10.1016/j.abst.2025.12.010
Idorenyin U. Umoren , Nnanake-Abasi O. Offiong , Niibari W. Vite
This study evaluated the antioxidant and neuroprotective effects of ethanol leaf extract and fractions of Launaea taraxacifolia against aluminum chloride-induced neurotoxicity in rats. Sixty-six female Wistar rats were divided into eleven groups, receiving either control treatment, aluminum chloride, donepezil, or different doses/fractions of the plant extract for 21 days. Aluminum chloride significantly reduced antioxidant enzyme activities (SOD, CAT, GPx) and increased lipid peroxidation (MDA). Co-treatment with the ethanol extract, dichloromethane, ethylacetate, and n-butanol fractions restored antioxidant defenses and reduced MDA levels, whereas the n-hexane and aqueous fractions showed little effect. These findings indicate that Launaea taraxacifolia contains bioactive compounds with protective effects against oxidative stress and neuronal injury, supporting its potential as a natural neuroprotective agent.
{"title":"Antioxidant and neuroprotective effects of Launaea taraxacifolia extract against aluminum-induced neurotoxicity","authors":"Idorenyin U. Umoren , Nnanake-Abasi O. Offiong , Niibari W. Vite","doi":"10.1016/j.abst.2025.12.010","DOIUrl":"10.1016/j.abst.2025.12.010","url":null,"abstract":"<div><div>This study evaluated the antioxidant and neuroprotective effects of ethanol leaf extract and fractions of <em>Launaea taraxacifolia</em> against aluminum chloride-induced neurotoxicity in rats. Sixty-six female Wistar rats were divided into eleven groups, receiving either control treatment, aluminum chloride, donepezil, or different doses/fractions of the plant extract for 21 days. Aluminum chloride significantly reduced antioxidant enzyme activities (SOD, CAT, GPx) and increased lipid peroxidation (MDA). Co-treatment with the ethanol extract, dichloromethane, ethylacetate, and n-butanol fractions restored antioxidant defenses and reduced MDA levels, whereas the n-hexane and aqueous fractions showed little effect. These findings indicate that <em>Launaea taraxacifolia</em> contains bioactive compounds with protective effects against oxidative stress and neuronal injury, supporting its potential as a natural neuroprotective agent.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 141-150"},"PeriodicalIF":0.0,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145924924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-29DOI: 10.1016/j.abst.2025.12.009
Kamlesh Sahu, Trilochan Satapathy, Poonam Sahu, Om Chandrakar
This section delineates the mechanistic framework linking chronic inflammation to carcinogenesis and critically explains how molecular biomarkers can be rationally exploited through nano-immunopharmacological strategies to enable precision therapy in inflammation-driven cancers. Chronic inflammation serves as a central driver of carcinogenesis, orchestrating tumor initiation, progression, metastasis and therapy resistance through highly intricate molecular networks. Inflammatory carcinomas such as inflammatory breast carcinoma, hepatocellular carcinoma and cholangiocarcinoma exhibit distinct gender- and region-specific prevalence, highlighting the dynamic interplay between host biology and tumor-promoting inflammatory micro-environments. At the molecular level, persistent pro-inflammatory cytokine signaling, notably IL-6 and TNF-α, in conjunction with activation of transcription factors NF-κB and STAT3, induces genomic instability, epigenetic reprogramming and epithelial-mesenchymal transition, collectively driving malignant transformation and aggressive phenotypes. The tumor micro-environment, enriched with immune subsets including tumor-associated macrophages, neutrophils and regulatory T cells, potentiates oncogenic signaling and fosters immune evasion. Emerging molecular biomarkers spanning cytokine signatures, immune checkpoints (PD-L1, CTLA-4) and epigenetic indicators offer critical prognostic value and therapeutic guidance. Cutting-edge nano-immunopharmacology enables precise modulation of these inflammatory axes by employing nanocarriers for cytokine inhibitors, immune modulators, RNA therapeutics and CRISPR-based interventions while minimizing systemic toxicity. By integrating mechanistic insights with translational strategies, receptor-guided nano-therapeutics emerge as a transformative approach to precision oncology, promising to redefine treatment paradigms, enhance therapeutic efficacy and overcome resistance in cancers fueled by chronic inflammation.
{"title":"Molecular biomarkers and nano-immunopharmacology in inflammatory carcinoma: Bridging mechanisms and therapeutic translation","authors":"Kamlesh Sahu, Trilochan Satapathy, Poonam Sahu, Om Chandrakar","doi":"10.1016/j.abst.2025.12.009","DOIUrl":"10.1016/j.abst.2025.12.009","url":null,"abstract":"<div><div>This section delineates the mechanistic framework linking chronic inflammation to carcinogenesis and critically explains how molecular biomarkers can be rationally exploited through nano-immunopharmacological strategies to enable precision therapy in inflammation-driven cancers. Chronic inflammation serves as a central driver of carcinogenesis, orchestrating tumor initiation, progression, metastasis and therapy resistance through highly intricate molecular networks. Inflammatory carcinomas such as inflammatory breast carcinoma, hepatocellular carcinoma and cholangiocarcinoma exhibit distinct gender- and region-specific prevalence, highlighting the dynamic interplay between host biology and tumor-promoting inflammatory micro-environments. At the molecular level, persistent pro-inflammatory cytokine signaling, notably IL-6 and TNF-α, in conjunction with activation of transcription factors NF-κB and STAT3, induces genomic instability, epigenetic reprogramming and epithelial-mesenchymal transition, collectively driving malignant transformation and aggressive phenotypes. The tumor micro-environment, enriched with immune subsets including tumor-associated macrophages, neutrophils and regulatory T cells, potentiates oncogenic signaling and fosters immune evasion. Emerging molecular biomarkers spanning cytokine signatures, immune checkpoints (PD-L1, CTLA-4) and epigenetic indicators offer critical prognostic value and therapeutic guidance. Cutting-edge nano-immunopharmacology enables precise modulation of these inflammatory axes by employing nanocarriers for cytokine inhibitors, immune modulators, RNA therapeutics and CRISPR-based interventions while minimizing systemic toxicity. By integrating mechanistic insights with translational strategies, receptor-guided nano-therapeutics emerge as a transformative approach to precision oncology, promising to redefine treatment paradigms, enhance therapeutic efficacy and overcome resistance in cancers fueled by chronic inflammation.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 151-171"},"PeriodicalIF":0.0,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145924925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study proposes a novel strategy for antiviral drug discovery by exploring endophytic fungi associated with Phyllanthus niruri, a medicinal plant traditionally recognized for its therapeutic value in liver disorders and viral infections. The research underscores the critical demand for cost-effective therapies for Hepatitis C Virus (HCV), particularly in low source settings which represents a major global health challenge with severe consequences like cirrhosis and hepatocellular carcinoma. The research focuses on identifying bioactive fungal metabolites with antiviral potential. Endophytic fungi were isolated from different tissues of P. niruri, followed by solvent extraction of the obtained isolates. Comprehensive phytochemical analysis was carried out to detect antiviral compounds such as lignans, flavonoids, alkaloids, tannins, coumarins, and saponins and the antioxidant property was evaluated by DPPH and ABTS assays demonstrated strong free-radical scavenging activity, supporting the therapeutic relevance of the extracts. The cytotoxicity assessment of the most promising fungal extract on HepG2 liver cell lines exhibited moderate effects at elevated concentrations, indicating a potential safety margin at lower doses for therapeutic applications. This investigation emphasizes the promise of endophytic fungi from Phyllanthus niruri as a significant source of natural antiviral agents, facilitating the pursuit of alternative treatments for HCV, offering a valuable lead toward the development of cost-effective therapeutic candidates.
{"title":"Bioscreening and phytochemical profiling of Phyllanthus niruri endophytic fungi with potential Anti-HCV applications","authors":"Kalyanasundaram Parvatham, Joysingh V. Kishonika Sri, Rajendiran Dharanika, Alagarsamy Atsaya, Velu Rajesh Kannan","doi":"10.1016/j.abst.2025.12.006","DOIUrl":"10.1016/j.abst.2025.12.006","url":null,"abstract":"<div><div>This study proposes a novel strategy for antiviral drug discovery by exploring endophytic fungi associated with <em>Phyllanthus niruri</em>, a medicinal plant traditionally recognized for its therapeutic value in liver disorders and viral infections. The research underscores the critical demand for cost-effective therapies for Hepatitis C Virus (HCV), particularly in low source settings which represents a major global health challenge with severe consequences like cirrhosis and hepatocellular carcinoma. The research focuses on identifying bioactive fungal metabolites with antiviral potential. Endophytic fungi were isolated from different tissues of <em>P. niruri,</em> followed by solvent extraction of the obtained isolates. Comprehensive phytochemical analysis was carried out to det<sub>ec</sub>t antiviral compounds such as lignans, flavonoids, alkaloids, tannins, coumarins, and saponins and the antioxidant property was evaluated by DPPH and ABTS assays demonstrated strong free-radical scavenging activity, supporting the therapeutic relevance of the extracts. The cytotoxicity assessment of the most promising fungal extract on HepG2 liver cell lines exhibited moderate effects at elevated concentrations, indicating a potential safety margin at lower doses for therapeutic applications. This investigation emphasizes the promise of endophytic fungi from <em>Phyllanthus niruri</em> as a significant source of natural antiviral agents, facilitating the pursuit of alternative treatments for HCV, offering a valuable lead toward the development of cost-effective therapeutic candidates.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 172-183"},"PeriodicalIF":0.0,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-18DOI: 10.1016/j.abst.2025.12.002
Christopher Busayo Olowosoke , Daniel Ogbonnaya Nwankwo , Chinedu Shedrach Izu , Prosper Obed Chukwuemeka
Artificial intelligence (AI) and biotechnology are two transformative fields converging to benefit STEM because of their reliance on data and models. The tools from both fields have redefined and improved translational performance of laboratory investigations on drug and biomarker-targeted discovery, drug design, drug development and drug delivery for personalized treatment. Although the long term merit of this integration of AI in biotechnology outweighs the demerit but is the current trend suitable and truly applicable for clinical intervention and therapy upgrades. In this article, we indicated how some key AI-biotech research is supporting accelerated novelty in biomarker-targeted discovery and drug delivery system (DDS) for disease management rather than merely incremental changes in 21st century.
{"title":"The integration of artificial intelligence and biotechnology in medicine: accelerating novelty in biomarker-targeted discovery and drug delivery systems","authors":"Christopher Busayo Olowosoke , Daniel Ogbonnaya Nwankwo , Chinedu Shedrach Izu , Prosper Obed Chukwuemeka","doi":"10.1016/j.abst.2025.12.002","DOIUrl":"10.1016/j.abst.2025.12.002","url":null,"abstract":"<div><div>Artificial intelligence (AI) and biotechnology are two transformative fields converging to benefit STEM because of their reliance on data and models. The tools from both fields have redefined and improved translational performance of laboratory investigations on drug and biomarker-targeted discovery, drug design, drug development and drug delivery for personalized treatment. Although the long term merit of this integration of AI in biotechnology outweighs the demerit but is the current trend suitable and truly applicable for clinical intervention and therapy upgrades. In this article, we indicated how some key AI-biotech research is supporting accelerated novelty in biomarker-targeted discovery and drug delivery system (DDS) for disease management rather than merely incremental changes in 21st century.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"8 ","pages":"Pages 137-140"},"PeriodicalIF":0.0,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145924923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}