Chemico-Biological Interactions最新文献

{"title":"Gaudichaudion H inhibits KRAS-mutant pancreatic cancer cell growth through interfering PDEδ-KRAS interaction","authors":"Lingyu Li ,&nbsp;Qingying Liu ,&nbsp;Yuyu Shao ,&nbsp;Shuo Wang ,&nbsp;Shuangyu Liu ,&nbsp;Xiaoning Wang ,&nbsp;Shuqi Wang ,&nbsp;Dongmei Ren","doi":"10.1016/j.cbi.2025.111529","DOIUrl":"10.1016/j.cbi.2025.111529","url":null,"abstract":"<div><div><em>KRAS</em> mutation results in higher proliferation rates and miserable prognosis of cancers. Targeting the interaction between KRAS and PDE6D provided an alternative strategy to overcome <em>KRAS</em>-mutant pancreatic cancers. Gaudichaudione H (GH) is a prenylated caged xanthone isolated from <em>Garcinia oligantha.</em> In this work, GH was selected as a potential anti-cancer compound by MTT screening of twelve prenylated xanthonoids from <em>G. oligantha.</em> Further studies demonstrated that GH inhibited proliferation of a panel of cancer cell lines and induced pancreatic cancer cell apoptosis. GH suppressed xenograft tumor growth accompanied with decreased phosphorylation of ERK and AKT. Binding with PDEδ and thus interfering the KRAS-PDEδ interaction was verified as the possible mechanism of GH. These findings implicated GH as a promising candidate for the treatment of pancreatic cancers with <em>KRAS</em> mutation, provided novel insight into the underlying mechanisms of GH-induced anticancer effects.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"415 ","pages":"Article 111529"},"PeriodicalIF":4.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting breast cancer cells with 2-indolyl-1,3,4-oxadiazole compounds by inducing apoptosis, paraptosis and autophagy","authors":"Pradeep M. Uppar ,&nbsp;Na Young Kim ,&nbsp;Keshav Kumar Harish ,&nbsp;Narasimha M. Beeraka ,&nbsp;Santhosh L. Gaonkar ,&nbsp;Mahendra Madegowda ,&nbsp;Gautam Sethi ,&nbsp;Kanchugarakoppal S. Rangappa ,&nbsp;Vladimir N. Nikolenko ,&nbsp;Arunachalam Chinnathambi ,&nbsp;Sulaiman Ali Alharbi ,&nbsp;Kwang Seok Ahn ,&nbsp;Basappa Basappa","doi":"10.1016/j.cbi.2025.111528","DOIUrl":"10.1016/j.cbi.2025.111528","url":null,"abstract":"<div><div>While 2-Indolyl-1,3,4-oxadiazole derivatives are recognized for their antibacterial properties, their potential as anticancer agents remains underexplored. This study investigates the anti-breast cancer properties of a novel 2-Indolyl-1,3,4-oxadiazole compound, 5l, focusing on its ability to induce apoptosis, paraptosis, and autophagy, and targeting poly (ADP-ribose) polymerase (PARP1), a critical enzyme in DNA repair. A series of 1,3,4-oxadiazole derivatives (compounds 5a-5m) were synthesized using an optimized multi-step process, enhancing reaction efficiency and yield. In silico molecular docking was used to determine binding efficacy of these derivatives. Lead compound, 5l, underwent cytotoxicity assays against MDA-MB-231, MCF-7, BT-474, and SK-BR-3 breast cancer cell lines, as well as the non-cancerous MCF-10A cell line. Molecular docking assessed the interaction of 5l with the PARP1 active site. Frontier molecular orbital (FMO) and molecular electrostatic potential (MESP) analyses were conducted to map electron distribution and identify reactive regions within compound 5l. The effects of 5l on cellular processes such as apoptosis, autophagy, and endoplasmic reticulum (ER) integrity were evaluated using live and dead assays, Annexin V staining, ER-tracker dye staining, and acridine orange assays. Western blotting analyzed apoptosis, paraptosis, and autophagy-related genomic instability. The optimized synthesis yielded high-purity 1,3,4-oxadiazole derivatives. Compound 5l displayed significant anticancer activity, with IC50 values of 63.7 μM, 29.1 μM, 50.3 μM, and 39.8 μM for MDA-MB-231, MCF-7, BT-474, and SK-BR-3 cell lines respectively, demonstrating its cytotoxic efficacy. Molecular docking revealed that 5l binds to PARP1 active site with a binding energy of −11.7 kcal/mol, indicating a strong interaction supporting its role as a PARP1 inhibitor. Annexin V assays, ER-tracker dye staining, and Acridine orange assays were used to assess apoptosis, ER integrity, and autophagy. 5l induced upregulation of cleaved PARP and downregulation of Alix-loaded proteins, alongside increased LC3-II expression, indicating autophagy-mediated genomic instability. Compound 5l exhibits potent anti-breast cancer activity through paraptosis, apoptosis, and autophagy-mediated genomic instability and by PARP1 inhibition with typically a low IC50 values, highlighting its potential as a therapeutic agent.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"415 ","pages":"Article 111528"},"PeriodicalIF":4.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143895961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptome profiling and DNA methylation analysis of human hepatocyte cell line HHL-16 in response to aflatoxin B1","authors":"Hang Wu ,&nbsp;Yun Yun Gong ,&nbsp;John Huntriss ,&nbsp;Michael N. Routledge","doi":"10.1016/j.cbi.2025.111531","DOIUrl":"10.1016/j.cbi.2025.111531","url":null,"abstract":"<div><div>Dietary exposure to aflatoxin B1 (AFB1) can cause acute aflatoxicosis and liver cancer, and is associated with immune suppression and growth impairment, but the molecular mechanisms of the health effects are not fully understood. A non-neoplastic human hepatocyte cell line 16 (HHL-16) was utilized to understand the effects of AFB1 on transcriptome and DNA methylation changes, identifying molecular pathways underlying toxicity and health effects. RNA sequencing and bioinformatic analysis (RNA-Seq) was applied to find the genes and pathways affected by AFB1. Bisulfite pyrosequencing was used to assess DNA methylation levels of CpG sites around promoter regions of gene of interest. RNA-sequencing revealed 280 significantly up-regulated and 296 significantly down-regulated genes in HHL-16 cells after 20 μg/ml AFB1 treatment for 24 h. KEGG pathway enrichment analysis indicated that differentially expressed genes (DEGs) were significantly enriched in the following pathways: cytokine-cytokine receptor interaction, NF-kappa B signalling pathway, TNF signalling pathway, IL-17 signalling pathway, amoebiasis, MAPK signalling pathway, and lipid and atherosclerosis. Further DNA methylation analysis found that there was significant hypomethylation at one CpG site of <em>CCL20</em> after 20 μg/ml AFB1 treatment on HHL-16 cells for 24 h. In conclusion, AFB1 modulates the expression of genes related to the pathways that play important roles in inflammatory response, growth, and cancers, and demonstrates the effects of AFB1 on DNA methylation.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"416 ","pages":"Article 111531"},"PeriodicalIF":4.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143894593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antitumor platinum(II) complex 56MESS binds to DNA G-quadruplexes, downregulates expression of c-MYC and k-RAS oncogenes, and triggers DNA damage in cancer cells","authors":"Jaroslav Malina ,&nbsp;Hana Kostrhunova ,&nbsp;Janice R. Aldrich-Wright ,&nbsp;Viktor Brabec","doi":"10.1016/j.cbi.2025.111534","DOIUrl":"10.1016/j.cbi.2025.111534","url":null,"abstract":"<div><div>Previous research indicated that the cytotoxic activity of the antitumor platinum(II) complex [Pt(1<em>S</em>,2<em>S</em>-diaminocyclohexane)(5,6-dimethyl-1,10-phenanthroline)]²⁺ (56ME<em>SS</em>) was not primarily attributed to DNA binding, despite the complex being confirmed to localize also in the nucleus. In this study, we have demonstrated that the antiproliferative activity of 56ME<em>SS</em> indeed involves DNA binding. Furthermore, in addition to binding duplex DNA, the complex also interacts with non-canonical secondary DNA structures, such as G-quadruplexes (G4s) and i-Motifs (iMs). This interaction leads to the suppression of G-regulated oncogene expression and disrupts key enzymatic processes associated with DNA, potentially contributing to DNA damage and the biological activity of 56ME<em>SS</em>. These findings build upon previously published results, revealing that the anticancer activity of 56ME<em>SS</em> is significantly more multifaceted than previously understood, involving multiple distinct mechanisms.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"416 ","pages":"Article 111534"},"PeriodicalIF":4.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143899502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of CYP2D6 gene expression in liver tissue: Variability in CYP2D6 mRNA levels within genotype-predicted metabolizer phenotype groups","authors":"Erika L. Meaddough ,&nbsp;Sara M. Sarasua ,&nbsp;Deborah Kunkel ,&nbsp;Luigi Boccuto ,&nbsp;Satishkumar R. Ganakammal ,&nbsp;Matt Moersen ,&nbsp;Christopher L. Farrell","doi":"10.1016/j.cbi.2025.111526","DOIUrl":"10.1016/j.cbi.2025.111526","url":null,"abstract":"<div><div>Pharmacogenetic (PGx) testing can be used to help guide drug therapy and decrease or avoid the risk of adverse drug reactions. <em>CYP2D6</em> is an important pharmacogene in pharmacogenomics testing panels. However, phenoconversion, whereby an individual's ability to metabolize a drug does not match the genotype-predicted metabolizer status, is a confounding factor to the accurate application of PGx testing results to patient care. To address this issue, <em>CYP2D6</em> expression between and within genotype-predicted CYP2D6 metabolizer phenotype groups was compared using WGS and RNA-Seq data from 134 normal liver tissue donors obtained from the GTEx program. Wide variability in <em>CYP2D6</em> mRNA levels was observed within metabolizer phenotype groups. The median expression level for ultrarapid metabolizers (UMs) was 738.9 TPM (transcripts per million; 196.8–778.9 TPM), 212.5 TPM (32.1–666.5 TPM) for normal metabolizers (NMs), 219.6 TPM for intermediate metabolizers (IMs) (22–389.8 TPM), and 121.2 TPM for poor metabolizers (PMs) (9.3–298.2 TPM). The PM and UM phenotypes were significant predictors of <em>CYP2D6</em> expression (<em>p</em> = 0.0004 and <em>p</em> = 0.019, respectively). Interestingly, expression of the gene encoding human serum albumin (<em>ALB</em>) was also a significant predictor of <em>CYP2D6</em> expression (<em>p</em> = 0.0003). Data from 50 patients with hepatocellular carcinoma obtained from the TCGA program showed no significant difference in expression between tumor tissue (median = 119.7 TPM, range 0.16–817.7 TPM) and normal matched tissue (median = 143.3 TPM, range 26.2–810.7 TPM). Transcriptional regulation of <em>CYP2D6</em> expression may contribute to differences in drug response and risk for CYP2D6 phenoconversion. Efforts to understand the role of gene expression to predict CYP2D6 phenoconversion may inform the use of PGx testing in the clinical setting.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"416 ","pages":"Article 111526"},"PeriodicalIF":4.7,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143941212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective effect of copper on neurotoxicity of TOCP in vivo","authors":"Brenda Rosales-Castro ,&nbsp;Isabel Bravo-Ontiveros ,&nbsp;Keyla Betanzos-Rau ,&nbsp;Kenia Nava-Aparicio ,&nbsp;Laura Ramírez-González ,&nbsp;Elizabeth Undiano ,&nbsp;Iván Flores-Pérez ,&nbsp;Eugenio Vilanova ,&nbsp;Antonio Monroy-Noyola","doi":"10.1016/j.cbi.2025.111527","DOIUrl":"10.1016/j.cbi.2025.111527","url":null,"abstract":"<div><div>A single or repeated dose of tri-ortho-cresyl phosphate (TOCP) induces in humans and animals a known neuropathy as organophosphorus-induced delayed polyneuropathy (OPIDP). This syndrome is related to the inhibition of neuropathy target esterase (NTE), causing signs and symptoms in the nervous system, such as ataxia and paralysis. Currently, there is no antidotal treatment for OPIDP. In the present study, the neuroprotective effect of Cu(II) on the acute <em>in vivo</em> neurotoxicity of TOCP is characterized. Adult hens (27 and 65 weeks old) were administered a single dose of 380, 500, 750, or 1000 mg/kg of TOCP dissolved in vegetable oil. One hour before, the animals were administered a single dose of 160 mg/kg of Cu(II) or vehicle by the same route. Twenty-four hours later, half of the animals (n = 5) in each group were decapitated to obtain the brain and blood (serum) for measuring NTE, acetylcholinesterase (AChE), cholinesterases (ChEs), and kidney and hepatic biochemical parameters (ALT, AST, creatinine, urea). The other half of the animals in each group were kept under observation for 21 days for clinical evaluation of OPIDP using a scale from 1 to 4. The 24-h brain NTE residual activity of all TOCP-treated groups was around 5 % (∼95 % inhibition) compared to the control group (vehicles). However, the group of hens treated with 380 mg/kg TOCP (27 weeks old) pre-treated with Cu(II) presented significantly higher brain NTE activity (p &lt; 0.05), which was around 55 %. This activity value correlated with the OPIDP clinical score over 21 days. Hens treated with TOCP showed an OPIDP score of 3, whereas those pre-treated with Cu(II) showed no signs of OPIDP. The protective effect of Cu(II) on brain NTE and serum ChEs inhibition levels was associated with the degree of OPIDP. The levels of both activities decreased with the increase in OPIDP score (1–4) due to higher TOCP doses and the age of the hens. Brain AChE inhibition ranged from 16 % to 43 %, and hens showed no cholinergic signs in any group. The dose of Cu(II) used in this <em>in vivo</em> study demonstrated a neuroprotective effect and did not induce adverse effects in the liver and kidneys. However, it will be necessary to carry out specific experimental studies to investigate the neuroprotective mechanism of Cu(II).</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"415 ","pages":"Article 111527"},"PeriodicalIF":4.7,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Guanylhydrazone and semicarbazone derivatives as potential prototypes for the design of cholinesterase inhibitors against Alzheimer's disease: biological evaluation and molecular modeling studies","authors":"Denise Cristian Ferreira Neto ,&nbsp;Joyce Sobreiro Francisco Diz ,&nbsp;Sulayne Janayna Araújo Guimarães ,&nbsp;Eduardo Mendes dos Santos ,&nbsp;Maria do Desterro Soares Brandão Nascimento ,&nbsp;Ana Paula Silva de Azevedo-Santos ,&nbsp;Tanos Celmar Costa França ,&nbsp;Steven R. LaPlante ,&nbsp;Claudia Jorge do Nascimento ,&nbsp;Josélia Alencar Lima","doi":"10.1016/j.cbi.2025.111515","DOIUrl":"10.1016/j.cbi.2025.111515","url":null,"abstract":"<div><div>Despite being present in many drugs, guanylhydrazones and semicarbazones are two functional groups that have been little investigated as potential therapeutic strategies for the treatment of Alzheimer's disease (AD). For this reason, we initiated the synthesis and evaluation of these compounds as potential anticholinesterase agents, aiming to offer new alternatives for drug development against AD. In the severe phase of AD butyrylcholinesterase (BChE) becomes the main enzyme responsible for the hydrolysis of acetylcholine (ACh). Therefore, in this project, we present the results of BChE inhibitory activity, enzyme kinetics, cytotoxicity, and molecular modeling studies for three guanylhydrazone and two semicarbazone derivatives that were previously synthesized and evaluated as acetylcholinesterase (AChE) inhibitors. Among the compounds tested, guanylhydrazones (<strong>1</strong>, <strong>2</strong>, and <strong>3</strong>) showed inhibitory activity against BChE, exhibiting a mixed non-competitive inhibition profile. Specifically, compound <strong>2</strong> (phenanthrenequinone) demonstrated superior inhibitory potency with an IC₅₀ of 0.68 μM, compared to compound <strong>1</strong> (acridinone) with an IC₅₀ of 3.87 μM, and compound <strong>3</strong> (benzodioxole) with an IC₅₀ of 101.7 μM. In contrast, semicarbazones (<strong>4</strong> and <strong>5</strong>) showed no BChE inhibition up to the highest concentration tested (300 μM). Importantly, all five compounds were found to be non-cytotoxic. Our results suggest that these compounds have potential as drug prototypes targeting different phases of AD. Compounds <strong>3</strong>, <strong>4</strong>, and <strong>5</strong> may be more effective in the early phase, when AChE activity remains high; compound <strong>1</strong> could be useful in the intermediate phase; and compound <strong>2</strong> appears particularly promising for the severe phase, when BChE plays a more dominant role.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"415 ","pages":"Article 111515"},"PeriodicalIF":4.7,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental and organ toxicity of fenpropimorph in zebrafish: Involvement of apoptosis and inflammation","authors":"Junhun Kweon ,&nbsp;Hojun Lee ,&nbsp;Junho Park ,&nbsp;Taeyeon Hong ,&nbsp;Garam An ,&nbsp;Gwonhwa Song ,&nbsp;Whasun Lim ,&nbsp;Wooyoung Jeong","doi":"10.1016/j.cbi.2025.111512","DOIUrl":"10.1016/j.cbi.2025.111512","url":null,"abstract":"<div><div>Pesticides are increasingly the focus as a prominent factor in environmental pollution. Fenpropimorph, a widely utilized morpholine fungicide, is a significant water pollutant. Because of its extensive usage, fenpropimorph is readily detected in diverse aquatic ecosystems. Despite its well-known toxicity to aquatic organisms, its toxicity to zebrafish development and accompanying mechanics remain unexplored. To assess fenpropimorph's toxicity and potential mechanism, we employed the zebrafish model, a representative tool in toxicological studies. Our results showed that exposure to fenpropimorph reduced embryonic viability during the early stages of development and reduced head and body size. Moreover, fenpropimorph triggered apoptosis, DNA fragmentation, and inflammation. Aberrations in the vascular network were observed in the <em>fli1:eGFP</em> transgenic zebrafish model. Additionally, neurotoxic impacts were further assessed using transgenic <em>olig2:dsRed</em> zebrafish, accompanied by a reduction of liver size and fluorescence intensity of <em>fabp10a:dsRed</em> zebrafish. mRNA expression analysis related to corresponding organ development further supported our data. Overall, our research suggests that fenpropimorph may cause aberrations in aquatic organisms.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"415 ","pages":"Article 111512"},"PeriodicalIF":4.7,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The use of Galleria mellonella in metal nanoparticle development: A systematic review","authors":"Razvan Vlad Opris ,&nbsp;Alina Mihaela Baciu ,&nbsp;Gabriela Adriana Filip ,&nbsp;Adrian Florea ,&nbsp;Carmen Costache","doi":"10.1016/j.cbi.2025.111511","DOIUrl":"10.1016/j.cbi.2025.111511","url":null,"abstract":"<div><div>Research on metal nanoparticles is crucial for their application in diverse fields, requiring detailed assessments of their effects and potential. <em>Galleria mellonella</em> larvae have emerged as a valuable model for studying the impacts of metal nanoparticles, offering ethical and logistical advantages over traditional models. This systematic review synthesizes evidence on the application of <em>Galleria mellonella</em> in evaluating the toxicity, distribution, and therapeutic potential of metal nanoparticles. Adhering to PRISMA guidelines, a comprehensive database search (MEDLINE, Embase, Cochrane, Scopus, Google Scholar, Science Citation Index Expanded) was conducted using keywords related to <em>Galleria mellonella</em> and metal nanoparticles. The SYRCLE's risk of bias tool (adapted for <em>G. mellonella</em>) was used for risk of bias assessment. Out of 1696 initially identified studies, 31 met the inclusion criteria, encompassing research from 2011 to 2024. The included studies effectively demonstrate <em>G. mellonella</em>'s capacity to model the toxicity of metal nanoparticles, their therapeutic potential in treating infections, and the impact on the innate immune response, bridging the gap between simpler <em>in vitro</em> assays and more complex mammalian models. <em>Galleria mellonella</em> stands out as a critical model for the early-stage development and evaluation of metal nanoparticles, particularly in assessing toxicity, therapeutic efficacy in infection treatment, and interaction with immune systems. This review underscores the larvae's role in metal nanoparticle research, advocating for its broader use to streamline development processes while minimizing ethical concerns.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"415 ","pages":"Article 111511"},"PeriodicalIF":4.7,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pyridoxine exerts antioxidant effects on kidney injury manifestations in high-fat diet-induced obese rats","authors":"Onanong Jaruan ,&nbsp;Sasivimon Promsan ,&nbsp;Laongdao Thongnak ,&nbsp;Nattavadee Pengrattanachot ,&nbsp;Nichakorn Phengpol ,&nbsp;Prempree Sutthasupha ,&nbsp;Anusorn Lungkaphin","doi":"10.1016/j.cbi.2025.111513","DOIUrl":"10.1016/j.cbi.2025.111513","url":null,"abstract":"<div><div>The modern diet contains a substantial level of fat which is believed to be one of the leading causes of the progression of kidney disease. Several studies have already demonstrated that consumption of a high-fat diet (HFD) induces inflammation and oxidative stress, causing activation of upstream mechanisms associated with kidney injury. For the prevention of such pathological events, a change in diet or the taking of nutritional supplements are recommended as alternative treatments. One of the forms of vitamin B6, pyridoxine (PN), has been shown to be an effective antioxidant and can also inhibit the formation of advanced-glycation end products (AGEs). In this study, the protective effects of PN (100 mg/kg/day for a period of eight weeks) against HFD-induced complications in obese rats were investigated. Rats fed on a HFD developed obesity which promoted inflammation, glucose intolerance, AGE receptor upregulation, oxidative stress, and kidney dysfunction. Intervention using PN mitigated obesity-related events and the impairment of kidney function by markedly reducing oxidative stress and also restoring the activity of antioxidant enzymes. Other studies have shown that some vitamin B6 derivatives inhibit the formation of AGEs but our study shows for the first time that PN exerted an antiglycative effect in this HFD-induced obesity model. Consequently, PN could potentially be a novel supplement for obese individuals to avoid kidney injury.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"415 ","pages":"Article 111513"},"PeriodicalIF":4.7,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}