Cytotechnology最新文献

{"title":"GP73 regulates autophagy and fibrotic responses in LX-2 cells through the PI3K/AKT/mTOR signaling pathway.","authors":"Shuangyan Luo, Ying He, Lianying Cai, Liu Liu, Yuxu Zhang, Lu Si, Qiuchen Cheng, Yunxiao Liang","doi":"10.1007/s10616-026-01082-9","DOIUrl":"https://doi.org/10.1007/s10616-026-01082-9","url":null,"abstract":"<p><p>Golgi protein 73 (GP73) has been identified as a potential biomarker for liver diseases. Numerous studies have consistently shown that GP73 expression is significantly elevated in the serum of patients suffering from various types of liver injury. Nevertheless, the underlying regulatory mechanisms by which GP73 contributes to liver fibrosis remain largely undefined. A liver fibrosis model was established by treating LX-2 cells with TGF-β1 for 24 h. LX-2 cells were subsequently cultured and subjected to various treatments, including transfection with plasmids (sh-NC, sh-GP73, oe-GP73) and administration of inhibitors (3-MA and LY294002). Western blot analysis was conducted to quantify protein levels of GP73, fibrosis markers, autophagy-related proteins, and components of the PI3K/AKT/mTOR signaling pathway. Quantitative PCR (qPCR) was utilized to measure GP73 mRNA expression across different samples. Additionally, immunofluorescence assays were performed to evaluate autophagic activity in LX-2 cells. Both mRNA and protein levels of GP73 in LX-2 cells were upregulated following TGF-β1 induction. Activation of the PI3K/AKT/mTOR pathway, as evidenced by increased phosphorylation of PI3K, AKT, and mTOR, along with enhanced autophagy, was observed upon treatment with TGF-β1 or GP73 overexpression. Conversely, silencing GP73 mitigated TGF-β1-induced fibrotic responses. Furthermore, inhibition of the PI3K/AKT/mTOR signaling axis using LY294002 alleviated GP73-mediated suppression of autophagy. The findings suggest that GP73 is associated with autophagy-related changes and fibrotic responses in LX-2 cells, potentially involving modulation of the PI3K/AKT/mTOR signaling pathway.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"211"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179823","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":"A prognostic model based on seven cell adhesion molecule-related genes to predict the prognosis of colorectal cancer.","authors":"Junchao Zhou, Zhan Shen","doi":"10.1007/s10616-026-01086-5","DOIUrl":"10.1007/s10616-026-01086-5","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a major contributor to cancer mortality. Cell adhesion molecules (CAMs) hold an essential role in CRC malignant progression. However, how to leverage CAMs-related genes to predict CRC prognosis and guide its treatment is still unclear. Gene expression data and clinical information of CRC patients were obtained from TCGA and GEO databases. Subsequently, a series of analyses were utilized to obtain 7 CAM-related feature genes and set up a prognostic risk model. The riskscore was obtained, and patients were stratified into high-risk (HR) and low-risk (LR) groups. Significant survival differences were observed (<i>P</i> < 0.001). According to the clinicopathological features and risk score, the ROC curve demonstrated that the riskscore showed good prognostic performance. Significant differences were in the immune infiltration of different groups. Patients in the LR group had a higher rate of gene mutation. Through enrichment analysis, the differential genes of the two groups were mainly involved in the Ras signaling pathway, signaling receptor activator activity, and growth factor activity. In addition, CGP-60,474, CMK, Dasatinib, and Imatinib may be targeted drugs in the HR group, while the targeted drugs in the LR group may be Erlotinib, Gemcitabine, JW-7-52-1, and Lapatinib. Expression validation of the 7 model genes was performed using both TCGA transcriptomic data and in vitro qRT-PCR, with consistent trends observed between the two approaches. In summary, the prognostic model can be applied to predict CRC prognosis.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01086-5.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"213"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13675168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215288","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":"Depression-related gene signature characterizes prognostic subtypes and therapeutic sensitivities in colorectal cancer.","authors":"Qiang Xu, Gang Hu, Ningjie Sun, Yikai Lou, Yuxuan Wu, Jianfeng Chen, Haiming Wu","doi":"10.1007/s10616-026-01075-8","DOIUrl":"10.1007/s10616-026-01075-8","url":null,"abstract":"<p><p>Depression substantially influences the occurrence, progression, and prognosis of colorectal cancer (CRC). Nevertheless, validated biomarker signatures that capture depression-associated prognostic signals in CRC remain to be established. This study aimed to develop a depression‑related gene (DRG) prognostic classifier and preliminarily evaluate its predictive biomarker utility in CRC. In the GSE39582 training cohort, we performed univariate Cox regression to identify overall survival (OS)‑associated DRGs sourced from previous studies. A candidate multi‑gene prognostic classifier was subsequently developed using least absolute shrinkage and selection operator (LASSO) regression followed by multivariate Cox analysis. The discriminatory performance of the signature was evaluated via Kaplan-Meier survival analysis and receiver operating characteristic (ROC) curves. To explore underlying biological patterns, we conducted comprehensive evaluations of the immune microenvironment, chemotherapeutic drug responsiveness, and functional enrichment among differentially expressed genes (DEGs) across risk‑defined subgroups. Furthermore, the potential biomarker relevance of signature genes in CRC was investigated through in vitro proliferation and migration assays. Among 702 DRGs, 71 exhibited significant associations with OS. The resulting 14‑gene signature demonstrated area under the curve (AUC) values of 0.64, 0.71, and 0.72 for 1‑, 3‑, and 5‑year OS in the GSE39582 training set. Patients classified into the high‑risk stratum showed markedly worse survival and expression profiles suggestive of reduced chemosensitivity to both 5‑fluorouracil and oxaliplatin. Among the 14 genes, METTL9 was identified as overexpressed in CRC tissues, showed association with unfavorable clinical outcomes, and exhibited enhanced proliferative and migratory capacities in CRC cells. We developed a risk stratification framework comprising 14 DRGs that showed moderate prognostic performance in CRC. This signature may serve as a candidate prognostic biomarker and highlights the potential relevance of depression-related molecular pathways in CRC, pending validation in prospective cohorts.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01075-8.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"201"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13594030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024000","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":"Antioxidant, genotoxic and cytotoxic effects of root extracts of <i>Astragalus microcephalus</i>: an assessment for alternative medicine.","authors":"Giray Buğra Akbaba, Füreya Elif Öztürkkan, Fikret Akdeniz","doi":"10.1007/s10616-026-01072-x","DOIUrl":"10.1007/s10616-026-01072-x","url":null,"abstract":"<p><p>The aim of this study is to evaluate the antioxidant, genotoxic and cytotoxic effects of root extracts of <i>Astragalus microcephalus</i> Willd. (<i>A. microcephalus</i>). Extracts were obtained using solvents such as ethanol, ethanol: n-hexane, n-hexane and methanol by Soxhlet extraction. The content of oil obtained from the n-hexane extracts of the plant was determined by Gas Chromatography with downstream Flame Ionization Detector (GC-FID) analysis. The antioxidant activity and total phenolic content of the extracts were determined by 2,2-diphenyl-1-picrylhydrazyl (DPPH) and Folin-Ciocalteu Methods, respectively. Genotoxic and cytotoxic properties of extracts at 50 and 100 µg/mL concentrations were investigated by Micronucleus (MN) and 3-(4,5-dimethylthiazol2-yl)-2,5-diphenyltetrazolium-bromide (MTT) assay, respectively. The roots of the plant contain an average of 2.53% oil. It was found that the most abundant fatty acid in the roots of the plant was linoleic acid. In addition, the roots of the plant contain palmitic, linolenic, 13,16-docosaadienoic, oleic and stearic acid. Methanolic extracts have the highest antioxidant activity and the richest in total phenolic content. All extracts obtained were determined to be genotoxic at 50 and 100 µg/mL. Methanol, ethanol: n-hexane and ethanol extracts of roots of <i>A. microcephalus</i> exhibit very low antioxidant activity even at high concentrations. Furthermore, except for the plant's ethanolic extract, all other extracts exhibit cytotoxicity at concentrations as low as 50 and 100 µg/mL. According to the results of this study, it isn't recommended to use the roots of <i>A. microcephalus</i> Willd. in the treatment of various diseases, considering their genotoxic and cytotoxic effects.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"198"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149008045","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":"USP18 is downregulated in an osteoporosis model and alleviates osteoblast inflammation and apoptosis by deubiquitinating TAK1 to inhibit the MAPK pathway.","authors":"Guoping Chen, Jinlong Liang, Yi Cui, Jiaheng Wei, Yongqing Xu","doi":"10.1007/s10616-026-01068-7","DOIUrl":"10.1007/s10616-026-01068-7","url":null,"abstract":"<p><p>Osteoporosis (OP) is a systemic metabolic disease associated with inflammation and apoptosis of osteoblasts. Ubiquitin-specific protease 18 (USP18) has been shown to participate in the progression of bone metabolic disorders; however, its role in osteoblast injury remains unclear. A rat OP model was established via bilateral ovariectomy (OVX). Pathological changes were observed using H&E and Masson staining, and Western blotting was used to detect the expression of related proteins. In vitro, an inflammatory injury model was constructed by inducing MC3T3-E1 mouse osteoblasts with 1 µg/mL LPS. CCK-8, EdU, flow cytometry, and Co-IP were utilized to validate the role of USP18 in osteoblast injury. OVX-treated rat femoral tissue samples exhibited severe inflammatory cell infiltration and bone damage. USP18 expression was significantly downregulated in OP rats and in LPS-stimulated osteoblasts. Overexpression of USP18 significantly increased cell viability and proliferation; upregulated the expression of osteogenesis-related protein markers (Runx2, ALP, and OCN); and reduced the levels of inflammatory factors (TNF-α and IL-6) and apoptotic proteins (Bax and cleaved caspase-3), thereby ameliorating LPS-induced osteoblast injury. Mechanistic studies revealed that USP18 binds to TAK1, removes K63-linked ubiquitination modifications on TAK1, and inhibits the activation of the p38/JNK-MAPK pathway. Notably, the MAPK activator anisomycin or TAK1 overexpression weakened the protective effects of USP18 on osteoblasts. USP18 inhibits MAPK pathway activation by deubiquitinating TAK1 and alleviates LPS-induced inflammation and apoptosis in osteoblasts. Furthermore, USP18 overexpression mitigates OP progression.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01068-7.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"203"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058972","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":"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":"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}