Cytotechnology最新文献

{"title":"Type IV collagen derived non-collagenous domain α6 (IV) NC1 and its derivative fragments inhibit endothelial cell proliferation and attenuates <i>in-vivo</i> chorioallantoic membrane angiogenesis.","authors":"Aravind Setti, Akbar Pasha, Venkata Krishna Kanth Makani, Manika Pal Bhadra, Smita C Pawar","doi":"10.1007/s10616-025-00709-7","DOIUrl":"10.1007/s10616-025-00709-7","url":null,"abstract":"<p><p>Targeting tumor angiogenesis with safe endogenous protein inhibitors is a promising therapeutic approach despite the plethora of the first line of emerging chemotherapeutic drugs. The extracellular matrix network in the blood vessel basement membrane and growth factors released from endothelial and tumor cells promote the neovascularization which supports the tumor growth. Contrastingly, small cleaved cryptic fragments of the C-terminal non collagenous domains of the same basement membrane display antiangiogenic effect. In the present study, full length α6(IV)NC1(Hexastatin) and its three subfragments α6S1(IV)NC1, α6S2(IV)NC1, and α6S3(IV)NC1 were validated for their pro-apoptotic and angio-inhibitory property. In order to construct the coding sequence of hexastatin and its three derivative partial peptide fragments were constructed with our proposed method, where the corresponding exons were amplified from the genomic DNA and then assembled together. Coding sequences were cloned and expressed using pLATE31 vector and recombinant proteins were purified with C-terminal His tag. The endogenous NC protein fragments of collagen IV were evaluated in vitro for their role in cytotoxicity on human umbilical vein endothelial cells (HUVECs). The results showed that the NC1 domain and its fragments inhibited the HUVECs cell proliferation, migration, invasion and induced apoptosis. The neovascularization inhibition was studied in in-vitro, via tube formation assay and in-vivo via the CAM Assay. The results showed that blood vessels and inter capillary network were inhibited in endothelial cells and also, in chick embryo treated with recombinant α6(IV)NC1 and its derivatives, except for α6S1(IV)NC1 and these endogenous protein inhibitors act as bio-therapeutics in inhibition of angiogenesis.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"47"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045806","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":"Long non-coding RNA HOXC-AS1 promotes the malignancy by sponging miR-195-5p with ANLN in esophageal cancer.","authors":"Yongchao Su, Feng Kuang, Hongwei Guo, Qu Chen, Yiquan Lai, Ran Jing, Lei Huang","doi":"10.1007/s10616-025-00711-z","DOIUrl":"10.1007/s10616-025-00711-z","url":null,"abstract":"<p><p>Long non-coding RNA HOXC cluster antisense RNA 1 (HOXC-AS1) exhibits elevated expression in gastric and prostate cancers, yet its involvement in esophageal cancer (EC) remains unexplored. This investigation assessed the expression patterns and functional implications of HOXC-AS1 in EC. Quantitative real-time PCR was employed to evaluate HOXC-AS1 expression in EC cell lines, while its impact on cell proliferation, migration, invasion, tumor growth, and metastasis was examined through MTT, EdU, transwell, wound healing assays, and animal models. Mechanistic insights into HOXC-AS1 were pursued using dual-luciferase reporter assays and RNA immunoprecipitation. Analysis of TCGA data demonstrated significant upregulation of HOXC-AS1 in EC tissues, consistent with its enriched expression in EC cell lines. Knockdown experiments revealed that suppressing HOXC-AS1 reduced proliferation, migration, and invasion of EC cells in vitro and inhibited tumor growth and metastasis in vivo. Mechanistically, HOXC-AS1 acted as a molecular sponge for miR-195-5p, with anillin actin-binding protein (ANLN) identified as a direct downstream target of miR-195-5p. Functional rescue experiments showed that inhibiting miR-195-5p or overexpressing ANLN counteracted the suppressive effects induced by HOXC-AS1 silencing on the aggressive phenotypes of EC cells. These findings establish HOXC-AS1 as a promoter of EC progression via regulation of the miR-195-5p/ANLN axis, suggesting its utility as a prospective therapeutic target for EC management.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"68"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515000","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":"Yunnan medicine Jiangzhi ointment alleviates hyperlipid-induced hepatocyte ferroptosis by activating AMPK and promoting autophagy.","authors":"Xin Hong, Haijing Liu, Hongli Sun, Yan Zhuang, Meizhen Xiao, Shaoping Li, Yandong Li, Ming Jing","doi":"10.1007/s10616-025-00737-3","DOIUrl":"10.1007/s10616-025-00737-3","url":null,"abstract":"<p><p>Nonalcoholic fatty liver disease (NAFLD) is a serious public health problem worldwide. The purpose of this study was to investigate whether Yunnan medicine Jiangzhi ointment (YMJO) can relieve the progression of NAFLD and to elucidate the specific mechanism involved. A NAFLD model was established in high-fat diet (HFD)-induced SD rats and free fatty acid (FFA)-induced BRL 3A cells. The expression of autophagy-related proteins and ferroptosis-related proteins was detected using Western blotting. The histopathological features of the livers of NAFLD rats were evaluated using hematoxylin and eosin (HE) and Oil Red O staining. The results revealed that in a successfully established HFD-induced NAFLD rat model, YMJO alleviated the progression of NAFLD, promoted autophagy, and inhibited ferroptosis. This regulatory mechanism is related to the activation of the AMPK pathway. Further study of the molecular mechanism via cell experiments revealed that YMJO activated FFA-induced liver cell autophagy through the AMPK signaling pathway and inhibited ferroptosis, thus alleviating the development of NAFLD. This study revealed that YMJO promotes phosphorylation by activating the AMPK pathway, enhances autophagy, ameliorates ferroptosis induced by high fat, and alleviates the occurrence and development of NAFLD.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"73"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11883071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585008","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":"In vitro and in vivo evidence of the effectiveness of gallic acid on glycerol-induced acute kidney injuries.","authors":"Khojasteh Hoseinynejad, Zahra Tafazzoli, Fereshteh Nejaddehbashi, Mehrnoosh Moosavi, Zahra Mansouri","doi":"10.1007/s10616-025-00706-w","DOIUrl":"10.1007/s10616-025-00706-w","url":null,"abstract":"<p><p>Because acute kidney injuries (AKI) are one of the critical health problems worldwide, studies on the risk factors, mechanisms, and treatment strategies seem necessary. Glycerol (GLY), known to induce cell necrosis via myoglobin accumulation in renal tubules, is widely used as an AKI model. This study aimed to evaluate the protective effects of gallic acid (GA) against GLY-induced AKI. The study utilized both in vivo and in vitro models. In vivo, healthy rats were divided into six groups: control (normal saline), GLY (10 mg/kg, intramuscularly), GLY + GA10 (10 mg/kg), GLY + GA50 (50 mg/kg), GLY + GA100 (100 mg/kg), and GA (100 mg/kg). GA was administered by gavage for seven consecutive days, followed by a single intramuscular injection of GLY. Kidney biomarkers, lactate dehydrogenase (LDH), oxidative stress markers, inflammatory indices, and histological parameters were assessed 72 h post-injection. In vitro, human embryonic kidney 2 (HK-2) cells were incubated with GLY and GA at different concentrations (30, 60, and 125 μg/ml) to evaluate cell viability, reactive oxygen species (ROS) production, oxidative stress, and inflammatory cytokines. GLY administration significantly elevated renal dysfunction markers, including blood urea nitrogen and creatinine, alongside oxidative stress and reduced cell viability. GA treatment improved kidney biomarkers, enhanced antioxidant enzyme activity, and reduced inflammatory cytokines. Histological analyses also showed improved kidney structural integrity in GA-treated rats compared to the GLY group. This study confirmed that GLY induces AKI through oxidative stress, inflammation, and structural damage. GA exhibited significant renal protective effects by enhancing antioxidant defenses and reducing inflammation. These findings support GA as a potential natural supplement for preventing or treating renal diseases.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"45"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045782","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 simplified in vitro disease-mimicking culture system can determine the angiogenic effect of medicines on vascular diseases.","authors":"SongHo Moon, Yuzuru Ito","doi":"10.1007/s10616-025-00736-4","DOIUrl":"10.1007/s10616-025-00736-4","url":null,"abstract":"<p><p>Many patients undergoing clinical regenerative treatments experience severe conditions arising from endothelial disruption. In chronic cardiac and perivascular diseases, deficiencies in vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), and heparin, which are essential for maintaining and activating endothelial cells, can lead to angiogenic dysregulation. Endothelial disruption caused by ischemic hypoxia and a deficiency in these factors is associated with many vascular diseases. However, their pathogenic processes remain unclear at the cellular level. Therefore, the present study aimed to develop a culture system that mimics the disease environment to test the effectiveness of drug candidates in restoring damaged blood vessels in chronic vascular diseases, including coronary artery disease and peripheral vascular disease. This study focused on VEGF, IGF, and heparin and developed a pseudo-disease culture system by pre-treating human umbilical vein endothelial cells (HUVECs) with a starvation medium (EGM-2™ medium lacking VEGF, IGF, and heparin) to examine the ability of HUVECs to form a traditional 2D vascular network. The results indicated that a deficiency in these proteins results in disruptions in tube morphogenesis. Moreover, the results suggested that dysregulation of the PI3K/AKT pathway plays a key role for in vascular disruption in HUVECs. The proposed pseudo-disease starvation system provides a simple way to visualize pathological disruptions to blood vessels and assess the efficacy of drugs for vascular regeneration.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00736-4.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"75"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585006","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":"β-sitosterol in Yijing Hugui decoction prevents cyclophosphamide-induced premature ovarian insufficiency via the AKT1/Nrf2 pathway.","authors":"Li Chen, Li Zeng, Shuyu Pan, Li Zu, Hongyan Pan, Li Fan","doi":"10.1007/s10616-025-00740-8","DOIUrl":"10.1007/s10616-025-00740-8","url":null,"abstract":"<p><p>Premature ovarian insufficiency (POI) is a condition marked by premature depletion of ovarian function, affecting a significant portion of women. The objective of this study is to assess the therapeutic efficacy of Yijing Hugui decoction (YJHGD) in the treatment of POI and to elucidate its pharmacological mechanisms. In this study, network pharmacology was used to identify key bioactive compounds in YJHGD, and the components were characterized using LC-MS. In vitro, we used KGN cells treated with cyclophosphamide (CP) to model POI. In vivo, a CP-induced POI mouse model was established. The in vitro therapeutic effects of β-sitosterol on CP-treated KGN cells were evaluated through various parameters. These parameters encompass cell viability, oxidative markers, antioxidant indexes, ATP concentration, intracellular ROS levels, apoptosis rate, and apoptosis-related protein expression. The in vivo therapeutic effects of β-sitosterol in POI mice were assessed through H&E staining, circulating reproductive hormone level detection, reproductive hormone receptor expression measurement, oxidative stress profile, and apoptosis assay. The potential protein target of β-sitosterol was identified utilizing molecular docking in conjunction with drug affinity responsive target stability (DARTS). β-sitosterol was identified as a major active component of YJHGD contributing to its therapeutic effects. In β-sitosterol-treated KGN human granulosa cells, oxidative stress and apoptosis were significantly reduced (<i>P</i> < 0.05). The interaction between β-sitosterol and AKT1 was verified. Furthermore, β-sitosterol significantly activated the AKT1/Nrf2 signaling pathway in vivo and in vitro (<i>P</i> < 0.05). AKT1 activator insulin significantly alleviated CP-induced oxidative stress (<i>P</i> < 0.05). Our results suggest that β-sitosterol inhibits oxidative stress and apoptosis by targeting AKT1 and activating the Keap1/Nrf2/HO-1 signaling. In vivo studies demonstrated that β-sitosterol significantly restored ovarian tissue damage in mice, reduced the circulating levels of reproductive hormones, downregulated the expression of reproductive hormone receptors, alleviated oxidative stress and ROS generation, and improved apoptosis (<i>P</i> < 0.05), which was achieved through the AKT1/Nrf2 pathway. In Conclusion, YJHGD possesses therapeutic potential for the treatment of POI. The active compound, β-sitosterol, demonstrated significant anti-POI effects through its interaction with AKT1, leading to the activation of AKT1/Nrf2 signaling pathway. This interaction contributes to the reduction of oxidative stress and the prevention of cellular apoptosis. Our results suggest that β-sitosterol may represent a novel therapeutic approach.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00740-8.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"76"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893954/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613859","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":"circDHX33 suppresses glycolysis, malignant proliferation, and metastasis in prostate cancer by interacting with RNA-binding protein IGF2BP2 to destabilize its protein.","authors":"XiangDong Liang, XiaoLiang Tan, Long Pei, ChunHui Dong","doi":"10.1007/s10616-025-00718-6","DOIUrl":"10.1007/s10616-025-00718-6","url":null,"abstract":"<p><p>Prostate cancer (PCa) is a malignant tumor characterized by dependence on androgens and enhanced glycolytic processes in response to the energy demands of rapid proliferation. This study delved into the role of circDHX33 interacting with IGF2BP2 in regulating the malignant behavior of PCa. circRNA expression data from PCa tissues and normal tissues were selected from the GEO database, and differentially expressed circRNAs were screened out. circDHX33 expression in clinical PCa samples was verified by RT-qPCR. Cellular experiments included cell culture, RNA interference and overexpression assays, as well as the use of Transwell migration invasion assay and EdU cell proliferation assay to assess the effect of circDHX33 on the proliferation and migration of PC-3 cells. In addition, its regulatory effect on energy metabolism in tumor cells was assessed by glycolysis assay. FISH assay, RNA pull-down, silver staining assay, and RIP were used to evaluate the interaction between circDHX33 and IGF2BP2. circDHX33 expression was significantly reduced in PCa tissues relative to normal tissues. Overexpression of circDHX33 significantly inhibited the glycolytic activity, proliferative capacity, and migratory and invasive abilities of PC-3 cells, and this effect was closely related to its reduction of IGF2BP2 protein stability. Knockdown of IGF2BP2 could reverse the malignant behavior of cells enhanced by circDHX33 knockdown. In addition, the direct intracellular interaction between circDHX33 and IGF2BP2 was verified. circDHX33 inhibits glycolysis and malignant proliferation in PCa through interaction with IGF2BP2, suggesting its potential as a potential therapeutic target.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"56"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11802939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381845","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":"Autotaxin regulates the expression and the activity of P-glycoprotein in lipopolysaccharide -activated microglial cells.","authors":"Mohammad Fayyad-Kazan, Zeina Soayfane, Wissam Faour, Hussein Fayyad-Kazan, Rana Awada","doi":"10.1007/s10616-025-00727-5","DOIUrl":"10.1007/s10616-025-00727-5","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDs), such as Alzheimer's and Parkinson's, are characterized by chronic inflammation and oxidative stress, often mediated by activated microglial cells. Microglia-induced neuroinflammation is essential to neuronal damage, driven by the overproduction of pro-inflammatory cytokines and reactive oxygen species. Autotaxin (ATX), a lysophospholipase D enzyme, can modulate inflammation through its enzymatic product lysophosphatidic acid (LPA). While previous studies highlighted ATX's anti-inflammatory properties, its impact on P-glycoprotein (P-gp), a key efflux transporter involved in drug resistance and neuroinflammation, remains not fully understood. The objective of this study was to explore how ATX modulates the expression and activity of P-gp in lipopolysaccharide (LPS)-activated and H2O2-stressed BV-2 microglial cells. Microglial cells were transfected with either an empty vector (EV) or an ATX cDNA vector (A +) and exposed to LPS (1 µg/mL) or H2O2 (100 µM). The mRNA expression levels of P-gp and pro-inflammatory cytokines were analyzed using qRT-PCR, and P-gp activity was assessed using the NBD-CSA fluorescence efflux assay. Our findings revealed that while LPS- and H₂O₂-treated microglial cells were characterized by an abnormal cellular morphology with long ramified processes, ATX overexpression restored the round shape morphology normally observed in the control untreated cells. Interestingly, ATX overexpression significantly reduced the mRNA levels of pro-inflammatory cytokines, such as TNF-<i>α</i>, in LPS- and H₂O₂-treated microglial cells. Moreover, ATX overexpression reduced both the mRNA levels and efflux activity of P-gp under inflammatory and oxidative stress conditions. These results suggest that ATX mitigates microglial activation and its downstream effects, highlighting its therapeutic potential in reducing neuroinflammation.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"58"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11822174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432667","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":"Mechanism underlying the role of the circRNA OMA1/miR-654-3p/RAF1 axis in children with inflammatory bowel disease.","authors":"Ping Zhang, Zhenhui Wang, Yufen Xu, Meirong Wu","doi":"10.1007/s10616-025-00703-z","DOIUrl":"10.1007/s10616-025-00703-z","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD), a chronic gastrointestinal disorder, often emerges during childhood and poses significant challenges due to its adverse effects on growth, development, and psychosocial well-being. Circular RNAs (circRNAs) have been implicated in the pathogenesis of diverse diseases. However, the specific biological role and mechanisms of circRNA OMA1 in children with IBD remain largely unexplored. This study investigates the functions and mechanistic pathways of circRNA OMA1 in the progression of IBD. Quantitative real-time PCR (qRT-PCR) was employed to quantify circRNA OMA1 and miR-654-3p expression levels in the serum of children with IBD and in HT-29 cells. Downstream miRNA and mRNA targets of circRNA OMA1 were predicted using StarBase and validated via luciferase reporter assays. An in vitro IBD model was established by treating the human colonic epithelial cell line (HT-29) with 2% dextran sulfate sodium (DSS). Cell viability and apoptosis were assessed using the MTT assay and flow cytometry, respectively. Expression of the apoptosis-related protein cleaved caspase-3 was analyzed via western blotting, and proinflammatory cytokine levels (TNF-α, IL-1β, and IL-6) were measured using ELISA. The expression of circRNA OMA1 was notably lower in the serum of children with IBD and in DSS-treated HT-29 cells than in healthy controls, whereas miR-654-3p expression was upregulated. Bioinformatics analyses revealed a direct interaction between circRNA OMA1 and miR-654-3p. Overexpression of circRNA OMA1 through plasmid transfection increased circRNA OMA1 levels and suppressed miR-654-3p expression in HT-29 cells under both basal and DSS-stimulated conditions. Conversely, transfection with a miR-654-3p mimic reversed these effects. Upregulation of circRNA OMA1 ameliorated DSS-induced injury in HT-29 cells by enhancing cell viability, reducing apoptosis, and downregulating cleaved caspase-3 expression. Moreover, circRNA OMA1 overexpression inhibited the secretion of inflammatory cytokines TNF-α, IL-1β, and IL-6. However, these protective effects were partially reversed by treatment with the miR-654-3p mimic. Additionally, miR-654-3p was shown to directly target RAF1, negatively regulating its expression. The proliferation-promoting and apoptosis-suppressing effects of miR-654-3p inhibitor treatment were mitigated by RAF1-siRNA. <i>Conclusion:</i> Upregulation of circRNA OMA1 alleviates DSS-induced colonic cell apoptosis and inflammation by modulating the miR-654-3p/RAF1 axis. These findings suggest that circRNA OMA1 could be a promising biomarker for the diagnosis and treatment of IBD.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00703-z.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"42"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045787","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":"The mechanism of curcumin protecting against IL-1β-induced oxidative stress and inflammation in chondrocytes via the Bmp2/Smad5/Runx2 pathway.","authors":"Jinlei Li, Weitong Liu, Tao Wang, Yanbo Wang, Guang Yang, Jiankun Chen, Yongsheng Xu, Jingfan Yang","doi":"10.1007/s10616-025-00731-9","DOIUrl":"https://doi.org/10.1007/s10616-025-00731-9","url":null,"abstract":"<p><p>A core role of chondrocyte survival/death has been suggested in the pathogenesis of osteoarthritis. We explored the underlying molecular mechanism of curcumin protecting against interleukin-1β (IL-1β)-induced chondrocyte injury via the bone morphogenetic protein 2 (Bmp2)/small mothers against decapentaplegic homolog 5 (Smad5)/runt-related transcription factor 2 (Runx2) pathway. Chondrocytes ATDC5 in vitro inflammatory model was established by IL-1β induction, and treated with curcumin, or Smad5 small interfering RNA. Levels of extracellular matrix (ECM) type II collagen (Col-II) and aggrecan, reactive oxygen species (ROS), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α) and IL-6 were determined by immunocytochemistry, kits and ELISA. Apoptosis and necrosis were assessed by Annexin V/PI and TUNEL. Matrix metalloproteinase 13 (MMP13), A disintegrin and metalloproteinase with thrombospondin 5 (ADAMTS5), Bmp2/Smad5/Runx2 expression and Smad5 phosphorylation levels were determined by qPCR and western blot. IL-1β-treated ATDC5 cells showed decreased Col-II, aggrecan in ECM and SOD and GSH-Px levels, as well as increased apoptosis and levels of MMP13, ADAMTS5, Bmp2, Runx2, ROS, COX-2, TNF-α and IL-6 and Smad5 phosphorylation (all <i>p</i> < 0.05), whilst curcumin treatment brought about the opposite trends, suggesting that curcumin inhibited oxidative stress, inflammatory response and apoptosis, and inactivated the Bmp2/Smad5/Runx2 pathway in IL-1β-treated chondrocytes. Additionally, Smad5 silencing also caused suppressed oxidative stress, inflammatory response and apoptosis in IL-1β-treated chondrocytes. Curcumin reduced IL-1β-induced chondrocyte oxidative stress, inflammation, and apoptosis, and increased ECM secretion by inactivating the Bmp2/Smad5/Runx2 pathway, thereby exerting a protective effect on injured chondrocytes.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"71"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11871223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540496","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}