Cytotechnology最新文献

{"title":"Cancer-associated fibroblast-derived CCL11 promotes prostate cancer malignancy by inducing epithelial-mesenchymal transition via CDK5.","authors":"Yu Wu, Xingyu Chen, Xinwei Yuan, Zhijun Chen, Xiaolin Guo","doi":"10.1007/s10616-026-01037-0","DOIUrl":"https://doi.org/10.1007/s10616-026-01037-0","url":null,"abstract":"<p><p>To elucidate the key role and underlying mechanisms of C-C motif chemokine ligand 11 (CCL11) in cancer-associated fibroblasts (CAFs)-mediated prostate cancer (PCa) progression. In this study, we analyzed the dataset GSE85606 and validated the upregulation of <i>CCL11</i> in CAFs using ELISA and qRT-PCR, demonstrating its strong correlation with established CAF biomarkers. Using CAFs-conditioned medium, recombinant human CCL11, specific siRNA, and <i>CDK5</i> plasmid or siRNA in PCa cell lines, we investigated the functional role of CCL11. RNA-seq and TCGA database analyses predicted a CCL11's downstream target (CDK5). Transwell, wound healing, and flow cytometry assays, along with Western blot, were employed to assess the effects of CCL11 on migration, invasion, apoptosis, and epithelial-mesenchymal transition (EMT) pathways. The results indicate that CCL11, predominantly secreted by PCa-derived CAFs, significantly enhances the migration and invasion of PCa cells, suppresses their apoptosis, and activates the EMT pathway, largely through regulating CDK5 expression. Collectively, our findings suggest that CAFs-derived <i>CCL11</i> may represent a potential therapeutic target for PCa.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01037-0.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"168"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13400532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WGCNA-based identification and experimental validation of TOP2A as a key regulator of ferroptosis in sepsis-associated acute respiratory distress syndrome.","authors":"Na Wang, Kang Li, Chuanyong Gong, Jie Bi","doi":"10.1007/s10616-026-01035-2","DOIUrl":"https://doi.org/10.1007/s10616-026-01035-2","url":null,"abstract":"<p><p>Sepsis-associated acute respiratory distress syndrome (SA-ARDS) is a severe disease with high morbidity and mortality. Emerging evidence indicates that ferroptosis plays a critical role in the development of SA-ARDS. However, the key regulatory targets and underlying molecular mechanisms remain to be further elucidated. Weighted gene co-expression network analysis (WGCNA) was performed based on the GSE66890 dataset to identify SA-ARDS-related gene modules. Candidate genes were screened by intersecting WGCNA module genes with ARDS-related targets from the GeneCards database and ferroptosis-related genes from FerrDb. An in vitro SA-ARDS model was established in HuLEC-5a cells using lipopolysaccharide (LPS). Cell viability, inflammatory cytokine levels, apoptosis, and ferroptosis-related parameters, including ROS, MDA, 4-HNE, and Fe²⁺ levels, were evaluated using MTT, ELISA, flow cytometry, and corresponding assay kits. The mRNA and protein expression levels were determined by RT-qPCR and Western blot. The transcriptional regulation of topoisomerase II alpha (TOP2A) by GATA binding protein 2 (GATA2) was verified using JASPAR prediction, chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays. All cellular experiments were performed using three independent biological replicates. WGCNA identified the salmon and cyan modules as significantly associated with SA-ARDS. Intersection analysis identified TOP2A as a key ferroptosis-related gene in SA-ARDS. TOP2A was significantly upregulated in LPS-induced HuLEC-5a cells. Knockdown of TOP2A markedly alleviated LPS-induced cellular injury, as evidenced by enhanced cell viability, reduced levels of inflammatory cytokines (IL-6, IL-8, TNF-α), decreased apoptosis rate, and lowered ROS and Fe²⁺ accumulation, reduced MDA and 4-HNE levels, restored GPX4 and SLC7A11 expression, and decreased ACSL4 expression, along with increased expression of endothelial barrier-related proteins. GATA2 directly bound to the TOP2A promoter and activated its transcription. TOP2A overexpression reversed the protective effects of GATA2 knockdown in LPS-induced HuLEC-5a cells. GATA2 transcriptionally activated TOP2A expression, which in turn promoted ferroptosis and exacerbated LPS-induced HuLEC-5a cell injury.</p><p><strong>Graphical abstract: </strong>GATA2 transcriptionally activates TOP2A to induce ferroptosis and exacerbate endothelial injury in SA-ARDS.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01035-2.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"167"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13400511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MGRN1 alleviates the progression of obesity-related acute lung injury by protecting lung epithelial cells through restoring mitochondrial function.","authors":"Yingping Wang, Liming Lu, Hui Jin, Jie Wu, Xin Li, Zhijuan Chen, Lisi Luo","doi":"10.1007/s10616-026-01038-z","DOIUrl":"10.1007/s10616-026-01038-z","url":null,"abstract":"<p><p>Acute lung injury (ALI) is a common respiratory disease worldwide, and obesity is a significant factor contributing to its progression. However, there is still a lack of effective clinical interventions specifically targeting this condition. This study aims to investigate the role of MGRN1 in obesity-related ALI. An obesity-related ALI mouse model was induced by a high-fat diet (HFD) and intratracheal instillation of lipopolysaccharide (LPS). An in vitro model was constructed using palmitic acid (PA) and LPS to stimulate mouse lung epithelial cells (MLE-12). Lung wet/dry weight ratio and HE staining were used to assess pathological changes in lung tissue. Cell damage was evaluated through CCK-8 and LDH release assays. Mitochondrial function was assessed via JC-1, Mito-Tracker Green, MitoSOX Red staining, and ATP content measurement. Additionally, RT-qPCR, Western blot, ELISA, immunofluorescence, and immunohistochemistry were employed to detect the expression of related genes and proteins.MGRN1 is downregulated in obesity-related ALI, and its overexpression alleviates LPS-induced lung histopathological damage in obese mice, reduces TNF-α, IL-1β, IL-6, ROS, and LDH levels, and inhibits PA-LPS-induced MLE-12 cell injury. Additionally, overexpression of MGRN1 restores mitochondrial function in PA-LPS-induced MLE-12 cells and suppresses PINK1/Parkin signaling pathway-mediated mitophagy. Further studies found that treatment with the PINK1 activator MTK458 attenuates the protective effect of MGRN1 overexpression on MLE-12 cells exposed to PA-LPS. MGRN1 restores mitochondrial function by inhibiting PINK1/Parkin-mediated mitophagy, thereby suppressing lung epithelial cell injury and ultimately alleviating obesity-related ALI. These findings suggest that MGRN1 may be a promising therapeutic target and that strategies aimed at restoring MGRN1 or pharmacologically restraining PINK1/Parkin-mediated mitophagy may offer a novel intervention for obese patients at risk of ALI, providing a theoretical basis for future clinical drug development.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01038-z.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"169"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13415410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydroalcoholic seed extract of Abelmoschus moschatus attenuates complete freund's adjuvant-induced arthritis in wistar rats: an in vivo pharmacological study.","authors":"Jitu Pawar, Tanvi H Desai, Vipul G Gajera, Devesh U Kapoor, Priyanka R Chaudhari, Dhara S Parekh","doi":"10.1007/s10616-026-01043-2","DOIUrl":"10.1007/s10616-026-01043-2","url":null,"abstract":"<p><p><i>Abelmoschus moschatus</i> i.a. a prostrate herb that is grown for its seed in tropical portions of Africa, South America, and Asia. It is a member of the Malvaceae family and also referred to Mushkdana. This plant has been reported for diuretic, antioxidant, antiproliferative, and antimicrobial activities along with its traditionally used in relieve spasms of the digestive track, aching joints and also considered as insecticide. Thus, anti-arthritic action of hydro-alcoholic extract of <i>Abelmoschus moschatus</i> seeds (EEAMS) were investigated in rats with arthritis caused by Complete Freund's adjuvant (CFA). In the present work powdered <i>Abelmoschus moschatus</i> seeds were extracted using 70% ethanol by the Soxhlet apparatus to prepare (EEAMS) and tested for phytochemical constituents. EEAMS was next tested for CFA induced arthritis in rats at dosages of 100, 200, and 400 mg/kg of weight by calculating paw volume, body weight, haematological and serum parameters, arthritic index, along with locomotor activity, antioxidant parameters and histopathological observation of ankle joints. EEAMS showed dose-related anti-arthritic effects by increasing body weight and reducing paw volume (100 mg/kg: 231 ± 5.59; 200 mg/kg: 236 ± 3.38; and 400 mg/kg: 237 ± 4.15) in association with control group (<i>P</i> < 0.05). It shown its considerable (<i>P</i> < 0.05) anti-arthritic action by elevate hemoglobin level and red blood cell, while concurrently declining C-reactive protein, erythrocyte sedimentation rate (ESR), WBC, and rheumatoid factor (100 mg/kg: 44.67 ± 3.37, 200 mg/kg: 40.05 ± 3.85, and 400 mg/kg: 36.39 ± 4.25) in different treatment group. The different dosages of EEAMS also improved dose dependent oxidative stress markers. Histopathological examinations also resulted in reduced joint damage in the feet. According to the results, EEAMS may be a viable therapeutic option of rheumatoid arthritis.</p><p><strong>Graphical abstract: </strong></p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"173"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13452792/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apoptosis induction by polyphenolic-rich extracts from <i>Flourensia cernua</i> and <i>Flourensia retinophylla</i> in human colon adenocarcinoma cells.","authors":"Diana Jasso de Rodríguez, Dennise Anahí Carrillo-Lomelí, J Omar Díaz-Rivas, Nuria E Rocha-Guzmán, Martha Rocío Moreno-Jiménez","doi":"10.1007/s10616-026-01041-4","DOIUrl":"10.1007/s10616-026-01041-4","url":null,"abstract":"<p><p>Colorectal cancer remains a leading cause of cancer-related death, and there is an urgent need for new therapies that can specifically induce tumor cell apoptosis. Plant polyphenols have emerged as promising alternatives for cancer treatment. <i>Flourensia cernua</i> and <i>F. retinophylla</i> are polyphenol-rich plants native to northern Mexico, known for their use in traditional medicine, and recently reported to have anti-inflammatory and antimicrobial properties; however, their anticancer effects remain poorly studied. This study aimed to evaluate the ability of polyphenolic extracts from <i>F. cernua</i> and <i>F. retinophylla</i> to induce apoptosis in HT-29 human colon adenocarcinoma cells in vitro and to explore the mechanisms of cell death triggered by these extracts. Polyphenolic extracts were prepared from dried leaves using ethanol and analyzed for antioxidant activity and polyphenolic composition. HT-29 cells were treated with different concentrations, and cytotoxicity was measured by MTT assay. Apoptosis was analyzed through intrinsic and extrinsic pathways, caspase activity, and detection of apoptosis-related proteins via Western blot and antibody array. Both <i>Flourensia</i> extracts are rich in polyphenols and exhibit high antioxidant capacity. Treatment with the extracts caused dose-dependent growth inhibition of HT-29 cells. <i>F. cernua</i> extract triggered cytochrome c and SMAC release, indicating activation of the intrinsic pathway, and also upregulated death receptor proteins and caspase-8, indicating engagement of the extrinsic pathway. <i>F. retinophylla</i> produced a weaker response, mainly modulating intrinsic-pathway markers. Both extracts also increased caspase-3 levels, consistent with engagement of apoptotic signaling. These findings demonstrate the potential of <i>Flourensia</i>-derived extracts as alternative anticancer agents with apoptosis-inducing potential in human colon adenocarcinoma cells.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"171"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13427710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148653104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding chromosomal instability in neutrophil signature in the pathogenesis of periodontitis: evidence from artificial intelligence-driven multi-omics and in vitro validation.","authors":"Bichu Zhang, Shixin Yao, Zhang Zhang, Feng Yi","doi":"10.1007/s10616-026-01046-z","DOIUrl":"10.1007/s10616-026-01046-z","url":null,"abstract":"<p><p>Periodontitis (PDT) is a chronic inflammatory disease driven by a dysregulated host immune response, with neutrophils playing a pivotal role. Chromosomal instability (CI) has emerged as a potent trigger of inflammation, yet its involvement in non-malignant diseases like PDT remains unexplored. Bulk RNA-seq data from gingival tissues between PDT patients and healthy control(HC) were analyzed via Limma framework to identify differentially expressed genes (DEGs) and CI-associated DEGs. WGCNA pinpointed a module correlated with neutrophil infiltration. Next, CI and neutrophil(CIN)-associated signature were acquired by integrating Limma and WGCNA results. NMF was used for molecular subtyping based on CIN-associated signature. A machine learning framework constructed a diagnostic model, with SHAP analysis identifying the hub gene based on PDT training and validation bulk profiles. Single-cell RNA-seq data validated cellular-level findings, and cutting-edge analytical framework inferred TFF3 functional impact at neutrophil of PDT patients in a temporal and spatial manners. The AI platform DrugReflector screened for therapeutic compounds for PDT patients, and in vitro assays examined the expression of hub gene. We identified 5 CI and neutrophil(CIN)-associated signature for PDT patients, which can guide the forecasting of PDT pathogenesis and PDT patient stratification. Besides, TFF3 can be considered as CIN-associated up-regulated pathogenic factor involved in PDT pathogenesis, which was mainly expressed in neutrophil. BRD-K92455082 as a candidate therapeutic agent targeting TFF3 for the treatment of PDT. This study first identifies a novel CIN-associated co-expression patterns in PDT. TFF3 can be considered as a candidate hub gene associated with a pro-inflammatory neutrophil state, providing new insights into the molecular taxonomy of PDT.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"188"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13525995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Engeletin alleviates MSU-induced inflammatory and tubular injury in vitro by targeting TLR4 and NFKB1.","authors":"Ruiwei Han, Chuanchao Wu, Xiaofeng Liang, Xiaoxue Xiang, Jiayi Wang, Jianhui Jiang, Qiuxia Lin, Li He","doi":"10.1007/s10616-026-01047-y","DOIUrl":"10.1007/s10616-026-01047-y","url":null,"abstract":"<p><p>The possible mechanisms of engeletin in hyperuricemic nephropathy (HN) has remained obscured; consequently, this investigation seeks to illuminate both the therapeutic potential and the mechanistic underpinnings of engeletin within the context of HN in vitro. The anti-HN mechanisms of engeletin were evaluated through in silico target identification and network pharmacology methodologies. Molecular docking was conducted using AutoDock Vina. RAW 264.7 macrophages and HK‑2 renal epithelial cells were treated with engeletin with or without monosodium urate (MSU) stimulation. Cell viability was assessed by the CCK‑8 assay. Migration was evaluated using Transwell assays. Pro‑inflammatory cytokines were measured by ELISA. In HK‑2 cells, mRNA levels of URAT1, GLUT9, OAT1, and ABCG2 were determined by qRT‑PCR, and XOD activity was measured using a commercial kit. TLR4 or NFKB1 overexpression was performed to confirm pathway involvement. TLR4 and NFKB1 were identified to be key targets for engeletin against HN. Molecular docking revealed stable binding of engeletin to TLR4 (‑6.6 kcal/mol) and NFKB1 (‑7.1 kcal/mol) with hydrogen bonds and anion pi interactions. Engeletin at 50 and 100 µM showed no cytotoxicity and significantly suppressed MSU‑induced RAW 264.7 cell migration and secretion of TNF‑α, IL‑6, IL‑1β, and MCP‑1. In HK‑2 cells, engeletin (100 µM) downregulated urate reabsorption transporters URAT1 and GLUT9, upregulated excretion transporters OAT1 and ABCG2, and inhibited XOD activity. Overexpression of TLR4 or NFKB1 markedly reversed all these effects. Engeletin can suppress cytokine release and macrophage migration, enhance renal urate excretion, and inhibite XOD activity in vitro, partly by targeting TLR4 and NFKB1.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01047-y.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"184"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BACH2 ameliorates lung injury in LPS-induced sepsis through activation of Nrf2 signaling.","authors":"Lihui Wang, Xiaoliang Ji, Shimin Dong, Qinglong Lu","doi":"10.1007/s10616-026-01024-5","DOIUrl":"10.1007/s10616-026-01024-5","url":null,"abstract":"<p><p>To explore the function and molecular mechanism of BACH2 in septic lung injury induced by lipopolysaccharide (LPS). We established LPS-induced septic lung injury models in mice and human bronchial epithelial BEAS-2B cells. By overexpressing/knocking down BACH2 and knocking down Nrf2, combined with pathological staining, molecular biology and cell experiment techniques, we detected the levels of lung tissue injury, inflammation and pulmonary fibrosis, and verified the regulatory relationship between BACH2 and Nrf2. In the lung tissues of mice with LPS-induced septic lung injury, the expression level of BACH2 was decreased in a time-dependent pattern. Overexpression of BACH2 significantly alleviated LPS-induced pathological injury of mouse lung tissues, inhibited neutrophil infiltration, and reduced the release of inflammatory cytokines and the degree of pulmonary fibrosis. BACH2 could directly bind to the -2000 ~ -1800 bp region of the Nrf2 promoter and upregulate its expression, and knockdown of Nrf2 completely reversed the lung protective effect of BACH2. BACH2 exerts anti-inflammatory and anti-fibrotic effects by directly binding to and activating the Nrf2 signaling pathway, thereby ameliorating LPS-induced septic lung injury. The BACH2/Nrf2 axis may serve as a candidate molecular target for further preclinical research on septic lung injury treatment.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01024-5.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"190"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13525998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nano guar gum triphenyl phosphonium conjugated rutin complex ameliorates hypertrophy in H9c2 cells via mitochondrial-mediated pathways.","authors":"R S Soumya, M S Ajay Krishna, Genu George, B S Sasidhar, K G Raghu","doi":"10.1007/s10616-026-01045-0","DOIUrl":"10.1007/s10616-026-01045-0","url":null,"abstract":"<p><p>Mitochondria-targeted antioxidants have emerged as a promising frontier in drug discovery, offering advantages over conventional antioxidants owing to recent technological advances. As the primary intracellular source of reactive oxygen species (ROS) mitochondria play a critical role in cellular health. Consequently, excessive mitochondrial ROS generation is heavily implicated in the pathogenesis of cardiovascular, neurodegenerative, and metabolic disorders. The etiopathogenesis of cardiovascular disease is mainly due to the dysfunction of mitochondria. Therefore, mitochondrial dysfunction is a novel curious target for developing new drug therapies. In this study, mitochondrial antioxidant (Ru-TPP-GGN) was prepared by incorporating triphenylphosphonium (TPP) conjugated rutin into guar gum nanoparticles (GGN) and was evaluated against angiotensin II (Ang II) induced hypertrophy in the H9c2 cell lines. The size of the synthesized Ru-TPP-GGN was about ≈ 15 nm, and it was subjected to detailed characterization to confirm its nano-characteristics. The cytoxicity analysis showed that the Ru-TPP-GGN was nontoxic to the cells. The cells treated with Ang II showed abnormalities in mitochondria with surplus superoxide generation, an increase in atrial natriuretic peptide (ANP) (125.75%↑) and brain natriuretic peptide (BNP) (82.75%↑) level, dissipation of mitochondrial transmembrane potential (ΔΨm), mitochondrial permeability transition pore (mPTP) opening, upregulation of transforming growth factor-β (TGF-β) protein expression, and alterations in the expression of proteins (OPA1, MFN1/2, FIS1, DRP1, and MFF) involved in mitochondrial biogenesis. Ru-TPP-GGN was found to avert the progression of hypertrophy via safeguarding mitochondrial integrity and dynamics. It is found to be a potential nanomaterial for further exploration for the development of mitochondrial antioxidant-based therapies against cardiac hypertrophy.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"189"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13526006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling berberine's multi-target mechanism in combating early-stage masld: a network pharmacology and in vitro study.","authors":"Shenglong Wei, Huajie He, Yong Xie, Youhua Wang, Xiaojiang Zhou","doi":"10.1007/s10616-026-01057-w","DOIUrl":"https://doi.org/10.1007/s10616-026-01057-w","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) poses a global health burden with limited therapies. Berberine (BBR) shows promise against MASLD, but its molecular mechanisms remain unclear. Network pharmacology predicted BBR-MASLD intersecting targets, followed by protein-protein interaction (PPI) network construction, GO/KEGG enrichment, and molecular docking. In vitro validation used FFA-induced HepG2 steatosis cells with Oil Red O staining, triglyceride assay, RT-qPCR, and Western blot for p-AKT/AKT. From 147 intersecting targets, six functional core targets were identified: AKT1, IL6, TP53, TNF, IL1B, and BCL2. Enrichment analyses implicated insulin resistance, lipid metabolism, and inflammation. Molecular docking confirmed strong BBR-core protein binding. In vitro, BBR dose-dependently reduced lipid accumulation and triglyceride levels, downregulated lipogenic (SREBP-1c) and pro-inflammatory (IL-6, IL-1β, TNF-α) genes, and restored insulin signaling (AKT1) and apoptosis-related (TP53) gene expression.BBR increased the p-AKT (Ser473)/total AKT ratio as shown by Western blot. BBR attenuates lipid accumulation and partially reverses steatosis-related transcriptional changes in an FFA-induced HepG2 model, including restoration of AKT1 signaling at both mRNA and protein phosphorylation levels. These findings suggest that BBR exerts protective effects againstearly hepatocellular steatosist hrough coordinated regulation of lipid metabolism, inflammation, and stress-related targets. This study provides a network-based rationale for further in vivo and mechanistic investigation in MASLD, and identifies potential pharmacodynamic biomarkers for future clinical trials.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01057-w.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"192"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13545187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}