Cytotechnology最新文献

{"title":"Effect of HOXB7 in promoting proliferation, invasion and migration of cervical cancer cells.","authors":"Jing Zhang, Juan Shen, Li Yuan","doi":"10.1007/s10616-026-00903-1","DOIUrl":"https://doi.org/10.1007/s10616-026-00903-1","url":null,"abstract":"<p><p>Cervical cancer (CC) represents the fourth most commonly diagnosed cancer and main cause of cancer mortality among women globally. We aim to investigate the mechanism of HOXB7 in CC cell progression, providing novel therapeutic implications for CC. Levels of HOXB7, miR-552-3p and IFITM1 in CC cells and tissues were measured by RT-qPCR and WB. After transfection of HOXB7 siRNA into CC cells, cell proliferation, invasion and migration were detected by CCK-8 method and transwell. The bindings of HOXB7 to miR-552-3p promoter and miR-552-3p to IFITM1 were analyzed. Effect of miR-552-3p and IFITM1 on the biological function of CC cells was detected in combined experiments. Results showed that the expression of HOXB7 and miR-552-3p was increased and the expression of IFITM1 was decreased. Cell proliferation, invasion and migration were reduced upon knockdown of HOXB7. Mechanically, HOXB7 bound and upregulated miR-552-3p expression, promoted the targeted binding of miR-552-3p to IFITM1, and reduced IFITM1 expression. miR-552-3p overexpression or IFITM1 downregulation reduced the inhibitory action of HOXB7 silencing on the proliferation, invasion and migration of CC cells. In conclusion, HOXB7 promotes the progression of CC cells via the miR-552-3p/IFITM1 axis.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00903-1.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"38"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118091","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":"SERPINA1 activation by RUNX1 drives microglial M2 polarization and reduces neuronal injury in a Parkinson's disease mouse model.","authors":"Keling Zhang, Shu Ding, Ting Li, Tangkun Yuan, Xiaoyu Cai","doi":"10.1007/s10616-025-00878-5","DOIUrl":"https://doi.org/10.1007/s10616-025-00878-5","url":null,"abstract":"<p><p>Microglial polarization plays a crucial role in Parkinson's disease (PD). This study explores how serpin family A member 1 (SERPINA1) suppresses neuroinflammation and alleviates neuronal damage in PD. Adeno-associated viruses were injected into mice to manipulate the expression of SERPINA1 or runt-related transcription factor 1 (RUNX1) in the substantia nigra, followed by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) modeling. Behavioral tests, histopathology (HE and Nissl staining), immunohistochemistry (IHC), immunofluorescence, and enzyme-linked immunosorbent assay were conducted to evaluate neuroinflammation and neuronal damage in mice. BV2 microglial cells were infected with lentiviruses overexpressing SERPINA1 and treated with 100 µM 1-methyl-4-phenyl-pyridinium (MPP)⁺. MPP⁺ increased pro-inflammatory cytokines and iNOS while decreasing anti-inflammatory cytokines and arginase-1 expression in BV2 cells. SERPINA1 and RUNX1 were upregulated in the SN of MPTP-induced mice. RUNX1 bound to the promoter region of SERPINA1 to induce its transcription. SERPINA1 or RUNX1 overexpression alleviated PD-related neuronal damage and neuroinflammation in mice and MPP⁺-induced inflammation in BV2 cells. SERPINA1 knockdown inhibited M2 polarization in the presence of RUNX1 overexpression. Taken together, RUNX1 transcriptionally activates SERPINA1, promoting microglial M2 polarization, suppressing neuroinflammation, and alleviating neuronal damage in PD.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00878-5.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"12"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12690037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145740299","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":"PLAU regulated by a m6A writer ZC3H13 plays the oncogenic role in oral squamous cell carcinoma.","authors":"Qingqing Cao","doi":"10.1007/s10616-025-00882-9","DOIUrl":"https://doi.org/10.1007/s10616-025-00882-9","url":null,"abstract":"<p><p>Oral squamous cell carcinoma (OSCC) is an aggressive malignancy with poor prognosis and limited therapeutic options. Plasminogen activator, urokinase (PLAU) is emerged as a potential key player in OSCC by bioinformatics analysis, but its function in OSCC have not been explored. Therefore, this study investigates its role and mechanism in OSCC progression, with a focus on its interaction with the N6-methyladenosine (m⁶A) writer ZC3H13. Differentially expressed genes in OSCC were identified through analysis of GEO datasets. A candidate oncogene was subsequently selected based on Gene Ontology enrichment analysis and validated using qRT-PCR in patient samples. The role of PLAU was examined by CCK-8, EdU, and transwell assays. In vivo tumorigenicity was evaluated using xenograft models. The relationship amongst PLAU and ZC3H13 was analyzed through correlation analysis, MeRIP, RIP, qRT-PCR, immunoblotting and mRNA stability assays. Finally, rescue experiments were conducted to validate the interactions between ZC3H13 and PLAU. PLAU upregulated in OSCC was identified as a candidate oncogene based on bioinformatic analysis and mRNA expression profiling. PLAU silencing suppressed cell proliferation, migration, invasion, and tumor growth, whereas its overexpression produced the opposite effects. Furthermore, ZC3H13 was positively correlated with PLAU expression. ZC3H13 overexpression enhanced m⁶A levels of PLAU to increase PLAU expression and mRNA stability. In addition, ZC3H13 overexpression partially rescued the suppressive effects of PLAU silencing on OSCC cells. In summary, these results illustrate that ZC3H13-mediated m⁶A modification increases PLAU mRNA stability and expression, thereby enhancing OSCC progression.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00882-9.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"11"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12686293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145721509","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":"Single-cell and machine learning-based analysis of the molecular mechanism of Banxia Xiexin Decoction in the treatment of gastric cancer.","authors":"Meng Li, Chao Song, Yanan Yu, Ming Dai","doi":"10.1007/s10616-025-00888-3","DOIUrl":"https://doi.org/10.1007/s10616-025-00888-3","url":null,"abstract":"<p><p>Gastric cancer (GC) is one of the most common malignant tumors worldwide. Banxia Xiexin Decoction (BXXXD) has a significant therapeutic effect on digestive system diseases, but its mechanism of action on GC is not yet clear. Using single-cell and bioinformatics to discover prognostic markers and Tumor Microenvironment (TME) components for GC, and further explore the molecular mechanism of BXXXD in treating GC through network pharmacology. KIF2C, KIF20A, KIF11, CDK1, CDC20, FN1, etc. could be used as diagnostic and prognostic markers for GC. The tumor microenvironment of GC mainly includes T cell, Neutrophil, B cell, Macrophage, Epithelial cell, Plasma cell, Stromal cell, Fibroblast, common myeloid progenitor cell. The core active ingredients of BXXXD synergistically regulate the MAPK signaling pathway, oxidative stress response, and apoptosis pathway, and multi-target reverse the pathological process of GC. We have established the correlation between the pathogenesis of GC's \"cold and heat disorder\" and modern pathological indicators (inflammation, oxidative damage, and cell apoptosis disorder) from the perspective of traditional Chinese medicine syndrome, providing a theoretical basis for the clinical application of BXXXD.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00888-3.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"23"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12775250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932608","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":"KLF2 inhibits keloid progression by targeting PI3K/AKT-mediated MMP-2/9 signaling.","authors":"Dan Yu, AoLin Zhao, ZhiGuo Wang","doi":"10.1007/s10616-025-00885-6","DOIUrl":"https://doi.org/10.1007/s10616-025-00885-6","url":null,"abstract":"<p><p>The anti-proliferation, anti-invasion, and anti-migration activities of KLF2 in keloid fibroblasts (KFs) and hypertrophic scar fibroblasts (HSFs) were investigated. KLF2 in normal skin (NF), keloid (KD), hypertrophic scar (HS) tissues, and cell lines was quantified using western blot and quantitative real-time polymerase chain reaction techniques. The processes of cell proliferation, migration, and invasion were observed in both KFs and HSFs, with pathway proteins linked to these processes pinpointed through western blot analysis. KLF2 in KD and HS tissues was lower than that in NF tissues. Enhancing KLF2 expression inhibited KF and HSF proliferation, migration, and invasion. MMP2, MMP-9, PI3K and p-Akt protein levels were inhibited in KFs with KLF2 overexpression. However, inhibition of PI3K and p-Akt protein levels was observed only in KLF2-overexpressed HSFs. In KFs with enhanced KLF2 expression, PI3K agonists eliminated the effect of KLF2 overexpression on cell migration and invasion. KLF2 inhibits the proliferation and migration of KFs by down-regulating MMP-2/9 through the PI3K/AKT pathway, suggesting that KLF2 may be a potential therapeutic target for KD. Hence, these findings offer novel perspectives on the function and molecular pathways of KLF2 in KD, as well as novel strategies for its clinical treatment.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00885-6.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"20"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12728153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833257","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":"Anti-atherosclerotic role of microRNA-218-5p <i>via</i> regulating the TNFRSF11A/NF-κB/NLRP3/caspase-1 pyroptosis pathway.","authors":"Chanjuan Wei, Junke Luo, Wenxuan Xiong, Junfeng Zhan","doi":"10.1007/s10616-026-00897-w","DOIUrl":"https://doi.org/10.1007/s10616-026-00897-w","url":null,"abstract":"<p><p>Atherosclerosis (AS) is linked to many cardiovascular disorders. We investigated the potential roles and mechanisms of microRNA (miR)-218-5p in AS. Primary mouse aortic endothelial cells (MAECs) were induced with ox-LDL, followed by various interventions including miR/gene overexpression and knockdown. An AS mouse model was established in ApoE^-/- mice and treated with miR-218-5p agomir. Serum lipid, inflammatory factor, interleukin (IL)-1β, IL-18, and pyroptosis-related protein levels as well as plasma anti-inflammatory IL-10 and TGF-β levels were determined. The results demonstrated that miR-218-5p overexpression decreased tumor necrosis factor receptor superfamily member 11 A (TNFRSF11A) protein level and ameliorated ox-LDL-induced MAEC pyroptosis. Furthermore, miR-218-5p impeded the nuclear factor (NF)-κB signaling and inactivated NOD-like receptor protein 3 (NLRP3)/caspase-1 <i>via</i> TNFRSF11A. NLRP3 activation partially reversed the impacts of miR-218-5p on pyroptosis. We observed augmented levels of serum total cholesterol, triglyceride, low-density lipoprotein cholesterol, and pro-inflammatory proteins, elevated levels of N-terminus of gasdermin D, TNFRSF11A, nuclear NF-kB p65, phosphorylated p65, NLRP3, and cleaved-caspase-1 proteins in aortic tissue, and reduced serum high-density lipoprotein cholesterol level and cytoplasmic NF-kB p65 protein level in AS-rendered mice. miR-218-5p agomir treatment reduced cell pyroptosis in aorta of AS model mice and improved AS. Briefly, miR-218-5p repressed TNFRSF11A, repressed the NF-κB signaling, and disrupted NLRP3/caspase-1 activation, thereby alleviating pyroptosis and contributing to the improvement of AS.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"32"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12827834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050844","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":"MiR-150-3p as a diagnostic biomarker and regulator of ferroptosis in preeclampsia via targeting FTH1.","authors":"Hao Geng, Pei Zhang, Limei Zhou, Xu Chen","doi":"10.1007/s10616-026-00896-x","DOIUrl":"https://doi.org/10.1007/s10616-026-00896-x","url":null,"abstract":"<p><p>Preeclampsia (PE) is a pregnancy-specific disorder characterized by new-onset hypertension after 20 weeks of gestation, and is associated with abnormal placental development, placental ischemia, and systemic endothelial dysfunction. There is new evidence that ferroptosis, a kind of cell death that depends on iron, plays a role in placental injury in PE. Unfortunately, our understanding of the regulatory mechanisms that underlie ferroptosis in PE is still limited. The purpose of this research was to examine miR-150-3p's function as a diagnostic biomarker and its function in controlling ferroptosis in the placenta of patients with PE via modulating ferritin heavy chain 1 (FTH1). We compared clinical indicators and placental ferroptosis markers in PE and normal pregnant women. Bioinformatics tools were used to predict miRNAs targeting ferroptosis-related genes, and experimental validation was performed in placental tissues and trophoblast cells. Dual-luciferase reporter assays and cell function analyses were conducted to examine the role of miR-150-3p and its target FTH1. PE placentas exhibited increased iron content and reduced expression of GPX4, SLC7A11, and FTH1. Bioinformatics identified miR-150-3p, miR-27a-3p, and miR-214-3p as top regulators of FTH1, SLC7A11, and GPX4, respectively. MiR-150-3p was markedly upregulated in PE and showed high diagnostic accuracy (AUC = 0.868). Functional assays revealed that miR-150-3p promotes ferroptosis in trophoblast cells by directly downregulating FTH1, leading to increased iron accumulation, lipid peroxidation, and oxidative stress. Our findings reveal a novel molecular pathway involving miR-150-3p/FTH1 in the development of PE, offering insights into potential biomarkers and therapeutic strategies targeting ferroptosis.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"31"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12819946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028651","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":"COL23A1 promotes tumor progression and glycolytic reprogramming in endometrial cancer via METTL14-m6A-YTHDF1 axis.","authors":"Huazhen Wu, Miao Ke, Xiaoli Feng, Zehan Li, Yuanwei Luo, Fanghui Bian, Jia Liao, Ruiming Tang","doi":"10.1007/s10616-026-00898-9","DOIUrl":"https://doi.org/10.1007/s10616-026-00898-9","url":null,"abstract":"<p><p>Endometrial cancer (EC) is one of the most common gynecological malignancies, and its progression is tightly linked to extracellular matrix (ECM) remodeling and metabolic reprogramming. Collagen type XXIII alpha 1 (COL23A1), a transmembrane collagen, has been implicated in several cancers, but its expression pattern, functional role and upstream regulation in EC remain unclear. Public datasets (TCGA, GTEx, cBioPortal) were analyzed to characterize COL23A1 expression, clinicopathological correlations and prognostic value. The biological functions of COL23A1 in EC cells were assessed by qRT-PCR, Western blotting, CCK-8, colony formation, flow cytometry, Transwell assays and Seahorse extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) measurements. Untargeted metabolomics and RNA immunoprecipitation (RIP) were used to interrogate glycolytic metabolism and m⁶A modification. Xenograft models were established to validate the in vivo effects of COL23A1. COL23A1 was significantly upregulated in EC tissues and correlated with advanced clinicopathological features and poor overall survival. Genetic silencing of COL23A1 suppressed EC cell proliferation, clonogenicity, migration and invasion in vitro, and inhibited tumor growth in vivo. At the metabolic level, COL23A1 knockdown disrupted glycolytic metabolism, leading to reduced glucose uptake, lactate production, expression of key glycolytic enzymes and ECAR, accompanied by a compensatory increase in OCR. Integrative bioinformatic and experimental analyses showed that METTL14 installs m⁶A modifications on COL23A1 mRNA, whereas the m⁶A reader YTHDF1 binds and stabilizes the modified transcript, thereby sustaining COL23A1 expression. Rescue experiments demonstrated that COL23A1 is required for METTL14- and YTHDF1-driven glycolytic reprogramming and oncogenic phenotypes in EC cells. COL23A1 acts as a previously unrecognized oncogenic driver in endometrial cancer, promoting tumor progression and glycolysis-dependent metabolic reprogramming through a METTL14-m⁶A-YTHDF1-COL23A1 axis. Targeting this m⁶A-dependent pathway may offer a promising therapeutic strategy for endometrial cancer.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00898-9.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"34"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12847561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146084761","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":"Dysregulation of miR-103a-3p in KGN cells and its targeting of KGN: potential role in polycystic ovary syndrome.","authors":"Xueqian Liu, Jingjing Ren, Yijiao Cheng, Yanjiao Liu","doi":"10.1007/s10616-026-00904-0","DOIUrl":"https://doi.org/10.1007/s10616-026-00904-0","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder. This study aims to investigate the expression of miR-103a-3p in PCOS and its potential molecular mechanisms. RT-qPCR was used to detect the levels of miR-103a-3p in the serum of PCOS patients, and to analyze its correlation with clinical indicators. The diagnostic value of miR-103a-3p for PCOS was evaluated through the ROC curve. Subsequently, the viability of KGN cells, inflammatory factors, and oxidative stress indicators were detected using CCK-8, ELISA, and oxidative stress detection kits, respectively. Finally, the targeting relationship between miR-103a-3p and PTEN was validated using dual luciferase reporter and RIP assays. The expression of miR-103a-3p in the serum of PCOS patients was significantly lower than that in the control group. miR-103a-3p demonstrates high sensitivity and specificity for the diagnosis of PCOS (AUC = 0.881). The expression level of miR-103a-3p is correlated with clinical indicators. In KGN cells, overexpression of miR-103a-3p significantly enhances cell viability, inhibits the secretion of inflammatory factors, and reduces oxidative stress levels, whereas inhibition of miR-103a-3p exhibits the opposite effects. The dual luciferase reporter assay and RIP experiment confirmed the direct interaction between miR-103a-3p and PTEN. In PCOS patients, miR-103a-3p is expressed at low levels and is closely associated with hormonal and metabolic indicators, potentially serving as an early diagnostic marker for PCOS. In vitro studies have found that miR-103a-3p may inhibit the progression of PCOS inflammation by targeting PTEN.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"41"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12872991/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146141367","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":"Synergistic hepatoprotection mediated by Tangeretin in <i>Naregamia alata</i>: <i>in vivo</i> and <i>in vitro</i> evidences.","authors":"Rajamathanky Hariharan, Rajasekaran Aiyalu","doi":"10.1007/s10616-026-00902-2","DOIUrl":"https://doi.org/10.1007/s10616-026-00902-2","url":null,"abstract":"<p><p>Our study focuses mainly on identifying the hepatoprotective activity of <i>Naregamia alata ethyl acetate (NAEA)</i> extract on Wistar rats. In addition, tangeretin was isolated, characterized and studied for <i>in vivo</i> and <i>in silico</i> approaches. D-GalN-induced hepatotoxicity rats were treated with 200 and 400 mg/kg of <i>NAEA</i> and its antioxidant and hepatoprotective activity was determined. The active constituent in the extract was isolated and spectral characterization was carried out. Cytoprotective, antioxidant and hepatoprotective activity of tangeretin was analyzed using MTT assay, DCFA-ROS assay and D-GalN induced toxicity in HepG2 cells. The anti-inflammatory activity of tangeretin in D-GalN treated cells was assessed by measuring the level of IL-6 and TNF-α via qRT-PCR. Molecular docking of tangeretin with the TACE enzyme was performed using AutoDock tools. Acute toxicity study in rats shows that <i>NAEA</i> exhibits no toxicity up to 4000 mg/kg. Hepatoprotective activity of the extract was confirmed by histopathological analysis and liver enzymes in d-galactosamine-induced hepatotoxicity rats treated with 200 and 400 mg/kg of <i>NAEA</i>. Spectral characterization reveals that the active constituent is tangeretin and MTT assay reveals IC₅₀ of 44.14 µM. 21.25 and 42.5 µM of tangeretin show antioxidant activity in DCFH-DA staining. The level of IL-6 and TNF-α were downregulated by tangeretin in HepG2 cells pretreated with D-Galactosamine. Molecular docking studies show that tangeretin binds to TACE with the binding energy of -9.13 kcal/mol and exhibits a low inhibition constant of 204.12 nM. Our findings show that the antioxidant, anti-inflammatory and hepatoprotective activity of <i>Naregemia alata</i> is due to the presence of tangeretin.</p><p><strong>Graphical abstract: </strong></p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00902-2.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 1","pages":"39"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118057","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}