Cytotechnology最新文献

{"title":"Hyperglycemia alters cell-cycle regulatory proteins in human amnion-derived mesenchymal stromal cells.","authors":"Betül İşiner, Gizem Korkmaz, Dijle Kipmen-Korgun, Hasan Berkan Sayal, Emin Türkay Korgun","doi":"10.1007/s10616-026-00966-0","DOIUrl":"10.1007/s10616-026-00966-0","url":null,"abstract":"<p><p>Human amnion-derived mesenchymal stromal cells (hAMSCs) represent a promising cell source for regenerative and experimental applications; however, culture conditions during in vitro expansion critically influence their biological properties. In this study, we investigated how hyperglycemic culture conditions affect the expression of key cell-cycle regulatory proteins in hAMSCs in vitro. Cells isolated from term placentas were exposed to normoglycemic (5 mM) or hyperglycemic (25 mM) glucose for 24 and 48 h, with equimolar mannitol included as an osmotic control. Cells exhibited mesenchymal stromal-like characteristics, supported by flow cytometric analysis and trilineage differentiation capacity. Protein levels of proliferation-associated markers (PCNA, cyclins D3, E, and B1) and cell-cycle inhibitors (p53, p57, and p27) were assessed by Western blotting. Exposure to high glucose (25 mM) for 48 h significantly downregulated PCNA, Cyclins D3, E, and B1. Interestingly, p53 and p57 were also reduced after 48 h under hyperglycemic conditions, while p27 expression remained unchanged. Notably, a decrease in p57 was detected even at 24 h, indicating early sensitivity to glucose stress. High glucose exposure was found to disrupt cell cycle regulation in hAMSCs in a time-dependent manner by suppressing both proliferative and inhibitory markers. These findings suggest that sustained hyperglycemia perturbs cell-cycle regulatory networks in hAMSCs and may limit their robustness in metabolically compromised environments.</p><p><strong>Graphical abstract: </strong></p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"91"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13087056/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721762","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":"Anticancer potential, antioxidant activity, chemical content, and enzyme inhibitory properties of <i>Inula aschersoniana</i> Janka, supported by an integrated network pharmacology study.","authors":"Abdülmelik Aras, Derya Taşkinsu Pamuk, İlhan Sabancilar, Alpaslan Bayrakdar, Ercan Bursal, Ömer Kiliç","doi":"10.1007/s10616-026-00955-3","DOIUrl":"10.1007/s10616-026-00955-3","url":null,"abstract":"<p><p>This study explores the biological and pharmacological potential of <i>Inula aschersoniana</i> Janka (<i>I. aschersoniana</i>) by utilizing both in silico computational and in vitro analyses, focusing on anticancer, antioxidant, and enzyme inhibitory activities. <i>I. aschersoniana</i> extracts were observed to have effective properties against breast cancer (MCF-7) and human colon adenocarcinoma (HT-29) cell lines compared to normal human umbilical vein endothelial (HUVEC) cell line. Also, effective antioxidant activity of the plant sample was determined by using several in vitro antioxidant methods. Furthermore, inhibitory effects of <i>I. aschersoniana</i> extracts against alpha-glucosidase (α-Gly) and glutathione S-transferase (GST) enzymes were evaluated. The IC₅₀ value of <i>I. aschersoniana</i> ethyl acetate extract was determined as 4.05 µg/mL for α-Gly and 1.67 µg/mL for GST. Similarly, IC₅₀ value of the ethanol extract was measured as 3.74 µg/mL for α-Gly and 2.71 µg/mL for GST. Also, main organic compounds of <i>I. aschersoniana</i> were detected to be vanillic acid, rutin, and naringin by HPLC technique. Finally, integrated network pharmacology, molecular docking, and molecular dynamics simulations were performed to elucidate the potential interactions between the active components of <i>I. aschersoniana</i> and genes associated with breast and colon cancer. To ensure reliability, molecular docking results were validated using re-docking and comparison with reference inhibitors or co-crystallized ligands. RMSD and RMSF analyses revealed that naringin, the major compound of <i>I. aschersoniana</i>, exhibited dynamically stable binding within the active sites of AKT1, EGFR, and PPARG proteins, with AKT1@Naringin and PPARG@Naringin complexes displaying a more stable dynamic profile. In this network pharmacology study, forty-five common targets between the major compounds of <i>I. aschersoniana</i> with breast and colon cancers were identified.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"92"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721783","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":"Exploring the laxative effects of emodin on constipation through chloride channel activation.","authors":"Shan-Shan Han, Qiang Chen, Li-Sheng Huo, Biao Tang, Liang Zang","doi":"10.1007/s10616-026-00984-y","DOIUrl":"https://doi.org/10.1007/s10616-026-00984-y","url":null,"abstract":"<p><p>Constipation, a prevalent gastrointestinal disorder, significantly impairs quality of life. Emodin, a bioactive anthraquinone found in traditional herbal remedies like <i>Rheum palmatum</i>, is empirically known for its laxative effects, yet its precise molecular mechanism remains incompletely understood. This study aimed to elucidate the laxative potential of emodin and delineate its underlying mechanism, with a specific focus on the activation of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel. This therapeutic effect was abrogated in W1282X cystic fibrosis mice lacking functional CFTR, demonstrating CFTR-dependency. In HT-29 human colonic epithelial cells, emodin activated the CFTR chloride channel detected by a fluorescence-based membrane potential assay in a concentration-dependent manner with a half-maximal effective concentration (EC₅₀) of 10⁻⁵·⁷ M and a maximal effect reaching 68.3% of that induced by the positive control, genistein. Mechanistic investigations revealed that emodin did not alter the total protein abundance of CFTR but significantly enhanced its phosphorylation. Pharmacological inhibition of the cAMP/protein kinase A (PKA) pathway attenuated emodin-induced CFTR activation and laxative effects. Consistently, emodin upregulated the mRNA expression of key cAMP/PKA pathway components, PRKACB and CREB1. In conclusion, our findings demonstrate that emodin alleviates constipation by activating the CFTR chloride channel. This effect is mediated through the cAMP/PKA signaling pathway, which enhances CFTR phosphorylation and channel activity, thereby promoting chloride-dependent fluid secretion into the colonic lumen. This study clarifies a pivotal molecular mechanism for emodin's laxative action and supports its therapeutic potential.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"104"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834679","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":"Stable mammalian expression of His-tagged prestin in Chinese hamster ovary cells.","authors":"Yasunori Donjo, Hisashi Sugimoto, Ryosei Motoo, Manabu Inaba, Tomokazu Yoshizaki, Michio Murakoshi","doi":"10.1007/s10616-026-00950-8","DOIUrl":"https://doi.org/10.1007/s10616-026-00950-8","url":null,"abstract":"<p><p>Chinese hamster ovary (CHO) cells are widely used for the stable production of recombinant proteins, including membrane proteins that require a mammalian cellular environment for proper folding and targeting. Prestin, a motor protein responsible for outer hair cell electromotility in the mammalian cochlea, is a multi-pass membrane protein whose structural and functional analyses require reliable expression systems capable of producing full-length protein. In the present study, we established CHO cell lines stably expressing full-length prestin with a C-terminal 6×histidine (His) tag using mammalian expression vectors driven by either the elongation factor-1α (EF1α) promoter or the cytomegalovirus (CMV) promoter. Following geneticin selection and limiting dilution cloning, multiple clonal cell lines were obtained and characterized by Western blotting, immunofluorescence microscopy and electrophysiological analysis. Seven clones expressing His-tagged prestin were identified. Quantitative Western blot analysis using a calibrated His-tagged reference protein demonstrated that the EF1α-driven system yielded higher-producing clones than the CMV-driven system, with a maximum estimated production of approximately 271 µg per 2 × 10⁹ cells. Immunofluorescence imaging confirmed membrane localization of prestin in expressing clones. Whole-cell patch-clamp recordings revealed nonlinear capacitance, indicating functional activity of the expressed protein. These results demonstrate that CHO cells provide a stable mammalian expression system for the production of full-length His-tagged prestin. The system enables reproducible protein production, quantitative expression evaluation and functional validation within a single cellular background, and may facilitate future biochemical, structural and functional studies of prestin and related membrane proteins.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00950-8.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"83"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13069067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671044","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":"Lysine-proline-valine peptide attenuates hepatic lipid accumulation through ROS-dependent regulation of the PPARγ pathway in HepG2 cells.","authors":"Ju-Yeon Lee, Jin Lee, Won-Kyo Jung, Jae-Young Je, Sei-Jung Lee","doi":"10.1007/s10616-026-00967-z","DOIUrl":"https://doi.org/10.1007/s10616-026-00967-z","url":null,"abstract":"<p><p>Hepatocellular steatosis, an early stage within the non-alcoholic fatty liver disease (NAFLD) spectrum, is characterized by excessive lipid accumulation and oxidative stress in hepatocytes. This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells. OA treatment markedly enhanced hepatic lipid deposition by upregulation of fatty acid synthase (FAS) expression. Treatment with KPV (100 µg/mL) significantly attenuated OA-induced lipid accumulation and suppressed FAS expression without inducing cytotoxicity. Mechanistic analysis revealed that KPV reduced reactive oxygen species generation, thereby preventing activation of extracellular signal-regulated kinase. KPV also downregulated AKT phosphorylation, leading to inhibition of mTORC1 phosphorylation under hepatic steatosis conditions. Furthermore, KPV regulated the phosphorylation of peroxisome proliferator-activated receptor gamma, a key transcription factor in <i>de novo</i> lipogenesis, thereby normalizing FAS expression. These findings suggest that KPV acts as an effective antioxidant regulator of lipogenic signaling and may hold potential as a therapeutic candidate for attenuating hepatocellular steatosis.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00967-z.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"98"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13125694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812067","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":"Resveratrol coordinates apoptosis and autophagy in hepatocellular carcinoma cells via p53 acetylation: An integrative network pharmacology and experimental validation study.","authors":"Hui Zhang, Huidong Zhang, Wei Li, Hong Zhang, Yang Xu, Wen Liu, Liya Bao, Siyu Zhou, Xiaoyu Zhang, Jiao Li","doi":"10.1007/s10616-026-00973-1","DOIUrl":"https://doi.org/10.1007/s10616-026-00973-1","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains a therapeutic challenge due to late-stage diagnosis and suboptimal response to standard therapies. Resveratrol, a plant-derived polyphenol, suppresses proliferation of HCC cells by inducing apoptosis and autophagy. However, the regulatory mechanism that integrates these two processes is poorly understood. This study aimed to elucidate how resveratrol coordinately regulates apoptosis and autophagy in HCC cells. Using integrated network pharmacology and QIAGEN Ingenuity Pathway Analysis (IPA), <i>TP53</i> was predicted as the central hub target gene of resveratrol in HCC, where it coordinated both apoptosis and autophagy. Molecular docking and molecular dynamics simulation confirmed direct and stable binding of resveratrol to p53 protein. Functional validation <i>in vitro</i> revealed that resveratrol significantly (<i>P</i> < 0.01) inhibited the viability of p53-wild-type HepG2 cells, accompanied by mRNA upregulation of pro-apoptotic and autophagy-related genes (<i>BAX</i>, <i>CASP9</i>, <i>CASP3</i>, <i>ATG</i>5), with concordant changes at the protein level (upregulated Bax and ATG5 proteins, increased ratios of Bax/Bcl-2, cleaved-Caspase 9/Caspase 9, cleaved-Caspase 3/Caspase 3, and LC3B-II/I, decreased p62 protein). These effects were strictly p53-dependent, as they were absent in p53-null Hep3B cells and significantly (<i>P</i> < 0.05) attenuated upon pharmacological inhibition of p53 in HepG2 cells. Mechanistically, resveratrol activated p53 not by increasing its protein level but by enhancing its acetylation at Lysine 382. This study established p53 acetylation as a critical switch through which resveratrol coordinately induced apoptosis and autophagy. These findings provide a mechanistic framework for anti-HCC effect of resveratrol and underscore the therapeutic relevance of p53 activation pathways in HCC.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00973-1.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"101"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13133310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812072","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":"FTO promotes bladder cancer progression and stemness-associated phenotypes.","authors":"Naping Wu, Xiaozhou He","doi":"10.1007/s10616-026-00971-3","DOIUrl":"https://doi.org/10.1007/s10616-026-00971-3","url":null,"abstract":"<p><p>The fat mass and obesity-associated protein (FTO), an N6-methyladenosine (m6A) demethylase, plays a crucial role in various cancers. This study investigates its expression and functional role in bladder cancer (BCa). Analysis of TCGA data and validation in BCa cell lines revealed that FTO is significantly overexpressed in bladder cancer tissues and is associated with poor overall and disease-free survival. Functional assays demonstrated that knockdown of FTO markedly increased global m6A RNA methylation and suppressed the proliferation, migration, invasion, and colony formation of BCa cells in vitro. Furthermore, FTO depletion significantly inhibited tumor growth and experimental liver colonization in nude mouse xenograft models. Mechanistically, transcriptomic analysis of FTO-high patient tissues and FTO-knockdown cells revealed a strong association between FTO and epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) pathways. Consequently, FTO knockdown impaired the self-renewal capacity of BCa cells and downregulated the expression of key stemness genes (CD133, CD44, Nanog, OCT4). These findings suggest FTO is a critical oncoprotein that promotes bladder cancer progression and stemness-associated phenotypes, highlighting its potential as a therapeutic target and prognostic marker.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"103"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834652","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":"Nuclear receptor subfamily 2 group F member 2 transcriptionally activates 14-3-3 epsilon to promote diffuse large B-cell lymphoma progression.","authors":"Liqian Yu, Yingwei Wang, Tiantian Li, Xiaoxue He, Wei Wang","doi":"10.1007/s10616-026-00965-1","DOIUrl":"https://doi.org/10.1007/s10616-026-00965-1","url":null,"abstract":"<p><p>Diffuse large B-cell lymphoma (DLBCL) represents the most prevalent form of non-Hodgkin lymphoma, distinguished by its aggressive clinical presentation and poor patient outcomes. This study investigated the role of nuclear receptor subfamily 2 group F member 2 (NR2F2) and 14-3-3 epsilon (YWHAE) in DLBCL progression. NR2F2 and YWHAE were highly expressed in DLBCL cell lines and tumor tissues of patients with DLBCL. Elevated expression of both genes correlated with advanced Ann Arbor stage and higher International Prognostic Index scores in DLBCL patients. Functional assays demonstrated that knockdown of NR2F2 or YWHAE suppressed DLBCL cell proliferation, migration, and invasion, as well as tumor growth in xenograft models. Mechanistically, NR2F2 transcriptionally activated YWHAE by binding to its promoter, thereby promoting phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling. Notably, treatment with a PI3K activator in YWHAE-silenced cells, or YWHAE overexpression in NR2F2-silenced cells, partially reversed the inhibitory effects on malignant behaviors of DLBCL cells. Collectively, these findings indicate that NR2F2 promotes DLBCL progression through transcriptional activation of YWHAE and subsequent activation of the PI3K/AKT pathway, suggesting a potential therapeutic target for DLBCL.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"96"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13103243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765132","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":"HOXD9 affecting glioma proliferation and invasion.","authors":"Zixuan Jing, Chenglong Li, Zefu Li","doi":"10.1007/s10616-026-00964-2","DOIUrl":"https://doi.org/10.1007/s10616-026-00964-2","url":null,"abstract":"<p><p>To investigate the expression of homology box D9 gene (HOXD9) in gliomas and its association with clinical features and prognosis, and to study the effect of HOXD9 gene on the proliferation and migration of glioma cells. HOXD9 knockdown models were constructed in U251 and U87-MG cell lines, and the effects of HOXD9 on glioma cell proliferation and invasion were verified using CCK8, plate cloning, Transwell, and migration assays. The expression levels of HOXD9 mRNA in TCGA database were also collected, and the prognostic value of HOXD9 was evaluated by plotting the survival curves. Gene set enrichment analysis (GSEA) was used to analyze the possible mechanism of HOXD9 gene in gliomas, and to analyze the correlation between the expression of HOXD9 gene and the immune cell infiltration of gliomas. In vitro experiments revealed that knockdown of HOXD9 expression inhibited the proliferation and migration of human glioma cells U251 and U87-MG. Bioinformatics showed that HOXD9 expression was up-regulated in gliomas, and HOXD9 expression correlated with overall survival (OS). GO and KEGG enrichment analyses revealed that HOXD9 was associated with multiple biological processes and signaling pathways. And the immune infiltration analysis about HOXD9 showed that HOXD9 was associated with a variety of immune cells, suggesting that HOXD9 might alter the immune microenvironment of the tumor. HOXD9 affects glioma cell proliferation and migration, and its expression is upregulated in glioma tissues, correlating with the prognosis of glioma patients. HOXD9 may serve as a potential therapeutic target and biomarker for glioma.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"84"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13069062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670986","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":"SIRT1 decreases Aβ-induced IL-1β production by suppressing NLRP3 inflammasome activation and M1 microglial polarization.","authors":"Sifan Long, Ruiqian Li, Jiaming Yang, Rong Cheng, Yanmei Wang, Yilong Dong","doi":"10.1007/s10616-026-00952-6","DOIUrl":"https://doi.org/10.1007/s10616-026-00952-6","url":null,"abstract":"<p><p>Microglia polarize into the proinflammatory M1 phenotype drive Alzheimer's disease (AD) pathogenesis through NLRP3 inflammasome-dependent maturation of interleukin (IL)-1β. Silent information regulator-1 (SIRT1) regulates a large number of cellular pathways and is related to aging and age-associated diseases, however, there were limited studies investigated whether SIRT1 can affect NLRP3 inflammasome and microglial activation and subsequent IL-1β production in AD. Here, we identified SIRT1 over-expression attenuated the release of IL-1β in amyloid-β (Aβ) treated microglia. Furthermore, our findings also revealed that NLRP3 inflammasome were less activated while the SIRT1 has been up-regulated. In addition, SIRT1 considerably alleviated the polarization of microglia toward to M1 phenotype mediated by Aβ, and the inhibitory on M1 polarization accompanied with the up-regulation of phosphorylated AMPK. This study demonstrated that SIRT1 can reduce IL-1β production by inhibiting the activation of NLRP3 and microglial phenotype toward M1, which suggesting SIRT1 may represent a potential strategy for modulating neuroinflammation in AD.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"85"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13070095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670991","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}