Cytotechnology最新文献

{"title":"Melatonin improves mitochondrial function and redox balance in human cartilage endplate-derived stem cells.","authors":"Pingfan Mo, Rongchun Chen, Linbo Sun, Yunsheng Chen, Jun Xiong, Yaohong Wu, Canhua Xu","doi":"10.1007/s10616-026-01025-4","DOIUrl":"10.1007/s10616-026-01025-4","url":null,"abstract":"<p><p>Mitochondrial oxidative stress is an important factor affecting the biological activity of stem cells under degenerative microenvironments. Cartilage endplate-derived stem cells (CESCs) are considered to participate in intervertebral disc homeostasis; however, their mitochondrial redox status under degeneration-related conditions remains incompletely characterized. In this study, human CESCs were isolated from patients with different degrees of intervertebral disc degeneration and used as an in vitro model to investigate mitochondrial oxidative stress. For intervention experiments, CESCs were treated with 100 µM melatonin for 24 h. Intracellular reactive oxygen species and mitochondrial superoxide were assessed using DCFH-DA and MitoSO™ Red, respectively. Mitochondrial membrane potential, ATP production, catalase and superoxide dismutase activities, and mitochondrial ultrastructure were evaluated. SIRT3 mRNA and protein expression were examined by quantitative real-time PCR and western blotting, and siRNA-mediated SIRT3 knockdown was used to explore its potential involvement in mitochondrial regulation. CESCs derived from advanced degeneration exhibited increased oxidative stress, decreased mitochondrial membrane potential, reduced ATP production, lower antioxidant enzyme activity, and greater mitochondrial ultrastructural damage. Melatonin treatment reduced intracellular ROS and mitochondrial superoxide accumulation and improved mitochondrial function. SIRT3 knockdown reduced SIRT3 mRNA and protein expression and partially attenuated the protective effects associated with melatonin. Melatonin increased SIRT3 mRNA expression, while SIRT3 protein expression was higher in the melatonin-treated group than in the SIRT3-siRNA group. These findings suggest that melatonin improves mitochondrial redox balance and mitochondrial function in human CESCs and that SIRT3 may participate in this regulatory process. The present study provides experimental evidence supporting a potential role for melatonin in modulating mitochondrial oxidative stress under degeneration-associated conditions.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01025-4.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"160"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13369075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148454857","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":"Phyto-synthesized silver nanoparticles from <i>Dendrobium heyneanum</i> and <i>Coelogyne mossiae</i>: a sustainable approach towards pharmaceutical applications.","authors":"Shivakrishnan Kaladharan, Sulaiman M, Meenaloshini Padmanaban, Subiya Showkat, Sivakumar Saroja Ramasubbu, Senthil Kumar Thiruppathi","doi":"10.1007/s10616-026-01028-1","DOIUrl":"10.1007/s10616-026-01028-1","url":null,"abstract":"<p><p><i>Dendrobium heyneanum</i> Lindl. and <i>Coelogyne mossiae</i> Rolfe, two critically conserved orchid species from the Western Ghats of India, remain among the least studied members of the Orchidaceae family due to their limited availability. In the present study, silver nanoparticles (AgNPs) were synthesized using aqueous extracts from in vitro-raised plants of <i>D. heyneanum</i> and <i>C. mossiae</i>, designated as DHSNP and CMSNP, respectively. The phyto-synthesized AgNPs were characterized using UV-visible spectroscopy, Fourier-transform infrared spectroscopy (FT-IR), X-ray diffraction (XRD), Dynamic light scattering (DLS), and Scanning electron microscopy (SEM). DHSNP and CMSNP exhibited UV peaks at 402 nm and 416 nm, respectively. FT-IR analysis identified functional groups such as alcohols, primary amines, aliphatic amines, and alkynes, while XRD confirmed their crystalline, Face-centered cubic structure. SEM revealed clustered particles with multiple-crystalline morphology. The phyto-synthesized AgNPs demonstrated notable antibacterial activity against <i>Staphylococcus aureus</i> (MTCC-7443), <i>Bacillus subtilis</i> (MTCC-7164) and <i>Pseudomonas aeruginosa</i> (MTCC-1688), with the highest zones of inhibition recorded against <i>P. aeruginosa</i> (27.59 mm for DHSNP and 26.00 mm for CMSNP). Both the phyto-synthesized AgNPs also exhibited promising antioxidant effects in the DPPH, Hydroxyl radical, Nitric oxide, and ABTS Scavenging assays. Furthermore, DHSNP reduced the cell viability of Human Glioblastoma U87-MG cells to 54.06%, whereas CMSNP reduced the viability of Human Melanoma SK-MEL-2 cells to 9.05%, accompanied by dose-dependent induction of apoptosis. Overall, the study demonstrates the antibacterial, antioxidant and anticancer activities of phyto-synthesized AgNPs from in vitro-raised <i>D. heyneanum</i> and <i>C. mossiae</i>, while establishing a sustainable approach for harnessing the pharmaceutical potential of unexplored orchid taxa.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"158"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13369119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148454859","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":"RBM15 enhances ILDR1 n6-methyladenosine methylation to accelerate gastric adenocarcinoma progression via an IGF2BP3-dependent manner.","authors":"Wei Hu, Xin Zhou, Bin Jiang, Jun Liu, Zi-Wei Li, Ming Song, Xin Zheng","doi":"10.1007/s10616-026-01022-7","DOIUrl":"10.1007/s10616-026-01022-7","url":null,"abstract":"<p><p>Gastric adenocarcinoma (GA), a major contributor to cancer-related mortality worldwide, is characterized by malignant progression driven by complex gene regulatory networks. However, the biological functions and N6-methyladenosine (m⁶A)-dependent regulatory mechanisms of RNA-binding motif protein 15 (RBM15), immunoglobulin-like domain-containing receptor 1 (ILDR1), and insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) in GA remain unclear. This study investigated their expression patterns, correlations, and regulatory mechanisms. Bioinformatics analyses were performed using TIMER, GEPIA, and TNMplot databases to predict the key regulatory axis in GA. RBM15-overexpression and ILDR1/IGF2BP3 knockdown models were established in two GA cell lines (AGS and SNU638) <i>via</i> transfection. Quantitative reverse transcription polymerase chain reaction and western blotting were used to assess gene and protein expression levels. Methylated RNA immunoprecipitation, RNA immunoprecipitation, and dual-luciferase reporter assay were performed to evaluate m⁶A modification and RNA-protein interactions. Messenger RNA stability was assessed using actinomycin D treatment, while Cell Counting Kit-8 and Transwell assays were employed to evaluate cell proliferation, migration, and invasion. In vivo xenograft experiments were conducted to investigate the effects of the RBM15/ILDR1 axis on tumor growth. RBM15 was significantly upregulated in GA tissues and positively correlated with ILDR1 expression. ILDR1 silencing markedly suppressed the cell proliferation, migration, and invasive capacity of GA. Mechanistically, RBM15 overexpression increased the m⁶A methylation level of ILDR1 mRNA. Furthermore, this methylation relied on the interaction between the m⁶A reader protein IGF2BP3 and ILDR1 mRNA. Notably, RBM15 overexpression effectively reversed the suppressive effects of ILDR1 depletion on malignant cellular phenotypes. Overall, RBM15 induced ILDR1 m⁶A methylation to enhance its stability in an IGF2BP3-dependent manner, thereby promoting GA progression. These findings provide novel mechanistic insights into GA pathogenesis and establish theoretical foundations for developing potential diagnostic biomarkers and targeted therapeutic strategies.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01022-7.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"150"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13328619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390175","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":"SP1-mediated NAT10 upregulation drives oral squamous cell carcinoma progression via ac4C-dependent SLC1A5 modification.","authors":"Lang Xu, Zhongwei Huang","doi":"10.1007/s10616-026-01010-x","DOIUrl":"10.1007/s10616-026-01010-x","url":null,"abstract":"<p><p>Oral squamous cell carcinoma (OSCC) is a prevalent malignancy in the head and neck region, accounting for 90% of all oral cancer cases. Despite advances in surgery and chemoradiotherapy, the molecular mechanisms driving OSCC progression remain incompletely understood, limiting the development of effective targeted therapies. Emerging evidence suggests that transcription factor Specificity protein 1 (SP1) and acetyltransferase N-acetyltransferase 10 (NAT10) may contribute to cancer progression, but their role in OSCC and potential regulation of the amino acid transporter solute carrier family 1 member 5 (SLC1A5) remain unclear. This study aimed to systematically investigate the SP1-NAT10-SLC1A5 regulatory network in OSCC development. The mRNA and protein expression levels were determined by reverse transcription-quantitative PCR (RT-qPCR) and western blotting, respectively. Cell proliferation was assessed using MTT and EdU assays, apoptosis was analyzed by flow cytometry, and cell invasion was evaluated using transwell assay. Enzymatic activity kits were employed to quantify key parameters of glutamine (Gln) metabolism. RNA immunoprecipitation (RIP) assay was used to detect the binding of NAT10 and SLC1A5 mRNA. Dual-luciferase reporter assay was performed to validate the direct regulatory interaction between SP1 and the NAT10 promoter region, followed by chromatin immunoprecipitation (ChIP) assay to assess SP1 occupancy on the NAT10 promoter. A mouse xenograft model was established for in vivo analysis. NAT10 expression was elevated in OSCC tissues and cells. NAT10 inhibition suppressed OSCC cell proliferation, invasion, and Gln metabolism and promoted apoptosis. Additionally, NAT10 mediated the ac4C modification of SLC1A5. Overexpression of SLC1A5 attenuated the effects of NAT10 suppression in OSCC cells. SP1 was identified as the upstream activator of NAT10 expression through transcriptional regulation analysis. Moreover, NAT10 inhibition impeded OSCC growth in vivo by regulating SLC1A5. SP1-induced NAT10 upregulation promoted OSCC advancement through ac4C-mediated SLC1A5 modification, providing new insights into OSCC treatment.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01010-x.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"140"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13291367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148327476","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":"Pyrogallol inhibits T cell lymphoma growth by mediating G₂/M phase cell cycle arrest, apoptosis, glycolysis and immune evasion: an implication of AKT pathway.","authors":"Abhishek Kumar, Mukesh Kumar, Siddharth Rai, Pratishtha Sonker, Ajay Kumar","doi":"10.1007/s10616-026-01034-3","DOIUrl":"10.1007/s10616-026-01034-3","url":null,"abstract":"<p><p>Pyrogallol, a polyphenolic compound, exhibits diverse activities, including antibacterial, antifungal, and antiviral effects; however, its anticancer potential has only been examined in a very few cancers and remains unexplored in T cell lymphoma. Hence, the present study is designed to elucidate the antitumor potential of pyrogallol against T cell lymphoma along with possible implication of modulated glucose metabolism and immune evasion. The experimental findings of this investigation show tumor-specific cytotoxicity of pyrogallol against T lymphoma cells. Further, pyrogallol has been shown to mediate G2/M cell cycle arrest by downregulating cyclin B1 and c-Myc expression, and induce apoptosis by altering ROS levels, mitochondrial membrane potential, and the expression of apoptosis regulators, namely Bcl2 and cleaved caspase 3, in T lymphoma cells. Furthermore, pyrogallol is observed to shift glucose metabolism towards oxidative phosphorylation by suppressing GLUT1, GLUT3, HKII, PKM2, PDK1, PDK3, and HIF-1α levels. Moreover, it suppresses the immune evasion ability of T lymphoma cells through deregulating 'do not eat me' and 'find me' signals, specifically PD-L1, CD-24 and CD-47, and S1P and LPC, respectively. Notably, the disrupted AKT pathway was found to play a critical role in pyrogallol-mediated T cell lymphoma growth inhibition. Overall, our investigation demonstrates that pyrogallol exerts tumor growth inhibitory effect in T lymphoma cells by modulating the cell cycle, apoptosis, glucose metabolism, and immune evasion in an AKT-dependent manner.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01034-3.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"161"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13379567/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497243","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":"CA7 overexpression enhances the anti-tumor effects of propofol in colorectal cancer via JAK2/STAT3 pathway.","authors":"Pingping Yin, Mengying Fan, Mengsi Yang, Chundong Liu","doi":"10.1007/s10616-026-01003-w","DOIUrl":"https://doi.org/10.1007/s10616-026-01003-w","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most common malignancies and remains a major contributor to cancer-related morbidity and mortality. Propofol, a commonly used intravenous anesthetic, has been verified to exert anti-tumor effects in CRC. However, the underlying molecular mechanism of propofol remains incompletely understood. This study aimed to investigate the role of carbonic anhydrase VII (CA7) in propofol-mediated the anti-tumor effects and to explore the involvement signaling pathways. The impact of propofol on CRC cell malignancy was assessed by cell and animal assays. qRT-PCR and western blotting were performed to detected the levels of mRNAs and proteins, respectively. The activation of CA7 promoter was assessed by luciferase reporter assay. Gain-of-function experiments were performed using CA7 overexpression vectors to assess the role of CA7 in propofol-treated CRC cells. The results showed that CRC cell survival, proliferation, migration, and invasion were suppressed by propofol. CA7 expression was elevated in CRC cells exposed to propofol treatment. CA7 overexpression enhanced the inhibitory effects of propofol on CRC cell malignancy. Mechanistically, propofol declined the activation of JAK/STAT3 pathway, which was further attenuated by CA7 overexpression in CRC cells. In vivo, propofol suppressed tumor growth and elevated CA7 expression in tumor tissues. Overall, CA7 overexpression potentiates the anti-tumor effects of propofol on CRC cell malignancy by suppressing JAK2/STAT3 pathway. These findings reveal a novel propofol/CA7/JAK/STAT3 regulatory axis in CRC and suggest that targeting CA7 may improve the therapeutic efficacy of propofol in CRC.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01003-w.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"134"},"PeriodicalIF":1.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13241344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197769","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":"Combination of paclitaxel with eugenol effectively enhances anticancer characteristics of paclitaxel on the A549 lung cancer cell line.","authors":"Hazim Dhaidan Malghooth Almalghooth, Mohammad Khalaj-Kondori, Mohammad Ali Hosseinpour Feizi","doi":"10.1007/s10616-026-01019-2","DOIUrl":"10.1007/s10616-026-01019-2","url":null,"abstract":"<p><p>Lung cancer, primarily non-small cell lung cancer (NSCLC), is a leading global cause of cancer mortality, driven by late diagnosis, drug resistance, and chemotherapy toxicity. Paclitaxel, a standard agent, stabilizes microtubules to induce G2/M arrest and apoptosis, but is limited by side effects such as neurotoxicity and resistance. Eugenol, derived from clove oil, offers anticancer benefits, including the induction of apoptosis and inhibition of metastasis. This study investigated the synergistic effects of Paclitaxel and Eugenol on A549 NSCLC cells, evaluating antiproliferative, pro-apoptotic, and anti-metastatic activities via cellular and molecular assays. A549 cells were cultured and MTT assay measured viability after Eugenol, Paclitaxel, and their combinations. Apoptosis was assessed by Annexin V-FITC/PI staining and flow cytometry. Cell cycle analyzed by PI staining and flow cytometry. qRT-PCR quantified <i>Bax</i>, <i>Bcl-2</i>, <i>Caspase-3</i>, <i>MMP-2</i>, <i>MMP-9</i> expression, and data analyzed by t-test/ANOVA. The MTT assay revealed Eugenol's IC₅₀ to be 257.9 µM and Paclitaxel's IC50 to be 8.485 µM after 24 h of incubation. Combination treatment with 100 µM Eugenol and 4 µM Paclitaxel synergistically enhanced cytotoxicity compared to individual agents. Flow cytometry demonstrated a significant increase in apoptosis with the combination and synergistic use of components. Cell cycle analysis revealed elevated sub-G1 populations at 11.8% for Eugenol, 20.3% for Paclitaxel, and 36.6% for the combination, which was prominent in the single treatments but reduced in the combination. qRT-PCR demonstrated downregulated anti-apoptotic <i>Bcl-2</i>, upregulated pro-apoptotic <i>Bax</i> and <i>Caspase-3</i>, and suppressed metastasis-related <i>MMP-2</i> and <i>MMP-9</i>, with effects most pronounced in the combination group. Eugenol enhances the efficacy of Paclitaxel on A549 cells by inducing superior apoptosis, disrupting the cell cycle, and inhibiting metastasis, suggesting potential strategies for reduced toxicity.</p><p><strong>Graphical abstract: </strong></p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"148"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13328530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390170","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":"Green light photobiomodulation modulates the temporal expression of neural and glial markers in mesenchymal stem cells.","authors":"Sajad Seyyedin, Hossein Fallah, Seyed Noureddin Nematollahi-Mahani","doi":"10.1007/s10616-026-01026-3","DOIUrl":"10.1007/s10616-026-01026-3","url":null,"abstract":"<p><p>Photobiomodulation (PBM) using light-emitting diodes (LEDs) has emerged as a promising approach to enhance differentiation potential of mesenchymal stem cells (MSCs). However, the temporal dynamics of neural-lineage marker expression following LED irradiation remain poorly understood. This study investigated the time-dependent effects of green LED irradiation on neural differentiation of human umbilical cord matrix-derived mesenchymal cells (hUCMs). Cells were exposed to green LED irradiation (530 nm, 1.59 J/cm²), retinoic acid (RA), and their combination (RA + LED). The expression of neural-lineage markers was evaluated by qRT-PCR and immunocytochemistry at days 7, 14, and 21 following neural induction of hUCMs. Green LED irradiation induced an early progenitor response, with nestin expression increasing on days 7 and 14 before declining by day 21. β-tubulin III and MAP2 showed transient increases, with the highest expression of β-tubulin III observed on day 14, particularly in the RA + LED group, whereas MAP2 expression increased primarily at days 7 and 14. Among the glial markers examined, Olig2 exhibited a delayed rise (days 14 and 21) in the LED and RA + LED groups, while GFAP increased in the RA and RA + LED groups at several time points. Overall, RA + LED treatment enhanced both the magnitude and timing of marker expression, making MAP2 and β-tubulin III responses earlier and more potent, but delaying the increase in glial-associated markers. These findings demonstrate that green LED-mediated PBM regulates neural-lineage commitment in a time-dependent manner, suggesting that day 14 may represent a favorable time point for harvesting preconditioned MSCs.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"153"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13346381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419516","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":"Naringenin as a potential immunomodulator for attenuating lung abnormal inflammation in Chronic Obstructive Pulmonary Disease (COPD) via the NF-κB/NLRP3/Caspase-1 Axis.","authors":"Yougen Zhang, Li Gu, Xiaoyang Zhang, Wei Ran, Yanfeng Yan, Hongwei Gu","doi":"10.1007/s10616-026-01032-5","DOIUrl":"10.1007/s10616-026-01032-5","url":null,"abstract":"<p><p>Pulmonary inflammation is a key feature of chronic obstructive pulmonary disease (COPD), contributing to disease progression and morbidity. However, the molecular mechanisms underlying therapeutic interventions remain to be fully elucidated. This study aimed to investigate the mechanisms of naringenin in modulating COPD-related pulmonary inflammation. Using an integrated approach combining network pharmacology, molecular docking, and in vitro/in vivo models, we systematically explored the effects of naringenin. Network pharmacology analysis identified NF-κB as a central target, which was validated through molecular docking and dynamics simulations showing stable binding between naringenin and NF-κB. In vitro, cigarette smoke extract-challenged lung epithelial cells treated with naringenin exhibited reduced cytotoxicity, downregulated TNF-α, phospho-NF-κB p65, and NLRP3 expression, inhibited Caspase-1 activation, and attenuated IL-1β maturation, and suppressed Gasdermin D cleavage. In vivo, naringenin-treated COPD mice displayed diminished pulmonary inflammatory cell infiltration, milder histopathological lung damage, decreased serum TNF-α/IL-1β levels, and inhibited activation of the NF-κB/NLRP3/Caspase-1 axis in lung tissue. Collectively, these findings reveal that naringenin alleviates COPD pulmonary inflammation and pyroptosis by targeting the NF-κB/NLRP3/Caspase-1 signaling cascade, providing mechanistic insights for traditional Chinese medicine-based COPD therapies.</p><p><strong>Graphical abstract: </strong></p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"156"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13356219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430021","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":"Identification and validation of dyslipidemia and glutamate metabolism-associated gene diagnostic and therapeutic repurposing signature for Acute myocardial infarction patients: insights from integrative bioinformatic and multi-omic studies.","authors":"Hanwei Zhao, Wenge Chen, Ran Cheng, Shuting Ren, Chuang Guo","doi":"10.1007/s10616-026-00979-9","DOIUrl":"https://doi.org/10.1007/s10616-026-00979-9","url":null,"abstract":"<p><p><i>Objective</i> Dyslipidemia and glutamate metabolism (DG) plays a crucial role in the pathogenesis of Acute myocardial infarction (AMI). Hence, deeper understanding of DG in AMI paves the way for the clinical applications of AMI. <i>Methods</i> In combination of PPI network and Limma framework, we first identified DG-associated shared differentially expressed genes (DEGs) from AMI patient bulk profile (GSE61144) and DG-associated gene list acquired from GEO and Genecard databases respectively. In another AMI patient bulk profile (GSE28454), we performed consensus clustering for classifying patient into 2 subgroups based on shared DG-related DEGs. By employing 2 machine learning algorithms (RF and SVM) in AMI patient training set (GSE109048), we identified DG-related hub gene, and then evaluated its diagnostic performance across GSE61144, GSE109048 and GSE66360(independent AMI patient bulk profile). Indeed, the molecular feature of DG-related hub gene was deciphered at GSE109048 and AMI single-cell transcriptomic profile (GSE269269). Finally, in vitro study illustrated the expression pattern of DG-related hub gene and DGIDB database with molecular docking proved the potential therapeutic framework for combating AMI. <i>Results</i> We discovered that DG-associated molecular subgroups and down-regulated expression gene signature CALR was diagnostic biomarkers for AMI, and Trentinoin should be considered as novel drug repurposing framework for the treatment of AMI. <i>Conclusion</i> We first pointed out that DG should be considered as diagnostic and therapeutic repurposing targets for the clinical translation of AMI, which can guide AMI patient personalized and precision medicine.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"127"},"PeriodicalIF":1.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13212843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053215","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}