Turkish Journal of Biochemistry最新文献

Downregulation of miR-1256 promotes breast cancer progression by targeting IL-22 and is associated with poor prognosis miR-1256下调通过靶向IL-22促进乳腺癌进展，并与不良预后相关

Turkish Journal of Biochemistry Pub Date : 2026-01-29 DOI: 10.1515/tjb-2025-0327

Yi Zhao, Qian Wang, Murong Liu, Wei Zhao

{"title":"Downregulation of miR-1256 promotes breast cancer progression by targeting IL-22 and is associated with poor prognosis","authors":"Yi Zhao, Qian Wang, Murong Liu, Wei Zhao","doi":"10.1515/tjb-2025-0327","DOIUrl":"https://doi.org/10.1515/tjb-2025-0327","url":null,"abstract":"Abstract Objectives Breast cancer (BC) poses a serious threat to women’s health, but its clinical prognosis is not ideal. miR-1256 has been shown to act as a tumor suppressor in various cancers, but its role in BC remains unknown. This study primarily explores the prognostic value of miR-1256 in BC. Methods The study included a total of 152 BC patients. RT-qPCR was employed to assay miR-1256 and interleukin-22 (IL-22) levels. Kaplan-Meier curves and Cox Proportional-Hazards Model (Cox) analysis were utilized to assess prognostic value. Cell Counting Kit-8 (CCK-8) and Transwell assays were used to study the proliferation and transfer capabilities of BC cells. Enzyme-linked immunosorbent assay (ELISA) assay for IL-22 protein content. The dual-luciferase reporter assay was employed to validate the relationship of miR-1256 with IL-22. Results miR-1256 level was significantly down-regulated in BC patients. The level of miR-1256 is closely related to clinical indicators, and high levels indicate a better prognosis. Overexpression of miR-1256 inhibits proliferation, migration, and invasion of breast cancer cells. Furthermore, IL-22 identified as a downstream target of miR-1256, is markedly up-regulated in BC patients and BC cells. Overexpression of IL-22 can reverse the suppression of malignant behavior in BC cells induced by miR-1256 mimic. Conclusions miR-1256 may inhibit malignant proliferation and transfer of BC cells by suppressing IL-22 levels. Furthermore, it holds promise as a potential target for clinical prognostication.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0327/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147905343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anti-lung cancer effect of Ornithogalum caudatum Jacq. via the CRHBP and regulation of M2 macrophage polarization 鸟尾草的抗肺癌作用。通过CRHBP调控M2巨噬细胞极化

Turkish Journal of Biochemistry Pub Date : 2026-01-08 DOI: 10.1515/tjb-2025-0215

Guanglei Wang, Yihua Zhang, Xikai Tao, Tingting Dong, Lei Du, Zekai Tang

{"title":"Anti-lung cancer effect of <i>Ornithogalum caudatum</i> Jacq. via the CRHBP and regulation of M2 macrophage polarization","authors":"Guanglei Wang, Yihua Zhang, Xikai Tao, Tingting Dong, Lei Du, Zekai Tang","doi":"10.1515/tjb-2025-0215","DOIUrl":"https://doi.org/10.1515/tjb-2025-0215","url":null,"abstract":"Abstract Objectives This study aimed to validate OCJ’s anti-lung cancer effect and CRHBP regulation mechanism in vitro . Methods The ETCM database was searched to identify the main components and specific targets of OCJ. According to the HPA database, the immunohistochemical (IHC) images of normal lung cells and lung cancer cells were screened. The CCK-8 assay and flow cytometry were employed to evaluate the impact of OCJ on cancer cell viability, proliferation, and apoptosis before and following CRHBP knockout. Finally, the mechanisms by which OCJ regulates M2 macrophages were explored. Results The major component of OCJ was Caudaside A, and the specific target was CRHBP, according to the ETCM database. CRHBP was found to be expressed at a lower level in lung cancer tissue and cells compared to normal tissue and cells. However, the expression level of CRHBP was increased by the addition of OCJ. In the cell functional assay, OCJ failed to effectively suppress cell proliferation or induce cell apoptosis following CRHBP knockdown. The inhibitory effects of OCJ on the M2 polarization markers of macrophages rescued by CRHBP suppression. Conclusions OCJ can promote the overexpression of CRHBP to inhibit the polarization of M2 macrophages, thus inhibiting lung cancer cell proliferation and inducing apoptosis.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0215/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147891571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The expression profile and clinical relevance of miR-486-5p in individuals with chronic periodontitis 慢性牙周炎患者miR-486-5p的表达谱及临床相关性

Turkish Journal of Biochemistry Pub Date : 2026-01-07 DOI: 10.1515/tjb-2025-0116

Shiliang Guo, Xingtao Wen, Huadan Jin, Fenglin Chen, Ling Li

{"title":"The expression profile and clinical relevance of miR-486-5p in individuals with chronic periodontitis","authors":"Shiliang Guo, Xingtao Wen, Huadan Jin, Fenglin Chen, Ling Li","doi":"10.1515/tjb-2025-0116","DOIUrl":"https://doi.org/10.1515/tjb-2025-0116","url":null,"abstract":"Abstract Objectives The development of chronic periodontitis (CP) is closely connected with the abnormal expression of microRNA. Here, we attempted to determine the levels of miR-486-5p in CP patients and to evaluate the function of miR-486-5p on the proliferation and apoptosis of human periodontal ligament cells (PDLCs). Methods A total of 80 patients with CP and 100 periodontally healthy individuals were enrolled. Gingival crevicular fluid samples (GCFs) were collected. PDLCs were stimulated with lipopolysaccharide (LPS) to establish an in vitro model of cells mimicking CP. The GCFs miR-486-5p expression was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The receiver operating characteristic curve was conducted to explore the diagnostic utility of miR-486-5p. Cell proliferation, apoptosis, and inflammatory factors were assessed by cell counting kit-8 assay, flow cytometry assay, and enzyme-linked immunosorbent assay. The interactions between miRNA and targets were investigated by dual luciferase reporter assay. Results The expression of miR-486-5p was increased in CP patients compared to controls. The area under the curve value was 0.878, which had a certain diagnostic value in CP. In vitro, cell experiments confirmed that the elevation of miR-486-5p diminished cell proliferation and enhanced apoptosis. Similarly, overexpression of miR-486-5p stimulated the release of inflammatory cytokines. PTEN was the target of miR-486-5p. Conclusions miR-468-5p had a certain value and significance as a biomarker for CP diagnosis, and its elevated expression correlates with the progression of the disease.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0116/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncRNA NBAT1 affects the progression of diabetic retinopathy by targeting miR-140-3p LncRNA NBAT1通过靶向miR-140-3p影响糖尿病视网膜病变的进展

Turkish Journal of Biochemistry Pub Date : 2026-01-07 DOI: 10.1515/tjb-2025-0405

Huili Cheng, Min Chen

{"title":"LncRNA NBAT1 affects the progression of diabetic retinopathy by targeting miR-140-3p","authors":"Huili Cheng, Min Chen","doi":"10.1515/tjb-2025-0405","DOIUrl":"https://doi.org/10.1515/tjb-2025-0405","url":null,"abstract":"Abstract Objectives Diabetic retinopathy (DR) is a serious threat to vision, with rising prevalence worldwide. Non-coding RNAs play a role in DR development. This study investigates how the lncRNA NBAT1/miR-140-3p axis regulates DR. Methods NBAT1 expression levels in serum were measured using RT-qPCR. Binding sites between miR-140-3p and NBAT1 were predicted using the LncRNASNP2 database. To simulate DR in vitro , a high glucose (HG)-induced ARPE-19 cell model was established. The expressions of NBAT1 and miR-140-3p under HG conditions were detected and the regulatory effect of NBAT1 on miR-140-3p was examined by dual luciferase reporter assay. After overexpressing NBAT1 and miR-140-3p in the HG model, TNF-α, IL-1β, and IL-6 levels were measured by ELISA. Results NBAT1 was significantly upregulated in DR patients compared to those with diabetes alone. The area under the ROC curve (AUC) of 0.7745 indicates its diagnostic potential for DR. Under HG condition, NBAT1 expression increased while miR-140-3p decreased. Dual luciferase reporter assay confirms that NBAT1 negatively regulates miR-140-3p. HG induction promoted inflammatory cytokine release in ARPE-19 cells, an effect that was amplified by NBAT1 overexpression. Importantly, transfection with miR-140-3p mimics reversed the pro-inflammatory effects induced by NBAT1. Conclusions NBAT1 is a risk factor for DR. In vitro studies show that NBAT1 worsens inflammatory responses in DR by negatively regulating miR-140-3p.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0405/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147896302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Distinct epigenetic analysis of mRNA 5-methylcytosine in the hippocampi of healthy young and aged mice 健康幼龄和老年小鼠海马中mRNA 5-甲基胞嘧啶的独特表观遗传分析

Turkish Journal of Biochemistry Pub Date : 2026-01-05 DOI: 10.1515/tjb-2025-0077

X. Zhang, Wenhui He, Sanwei Jiang, Junmei Li, Qinbin Hu, Chengzhang Li, Lingtong Zhi, Chengbiao Lu

{"title":"Distinct epigenetic analysis of mRNA 5-methylcytosine in the hippocampi of healthy young and aged mice","authors":"X. Zhang, Wenhui He, Sanwei Jiang, Junmei Li, Qinbin Hu, Chengzhang Li, Lingtong Zhi, Chengbiao Lu","doi":"10.1515/tjb-2025-0077","DOIUrl":"https://doi.org/10.1515/tjb-2025-0077","url":null,"abstract":"Abstract Objectives To profile the mRNA m 5 C modification landscape in hippocampi from young and aged mice. Methods MeRIP-seq (Methylated RNA Immunoprecipitation Sequencing) technology was conducted to profile m 5 C-tagged peaks and genes in young and aged hippocampi. M 5 C methylation-related enzymes were detected using Western blot. Results The numbers of m 5 C methylation peaks and genes were increased during aging. Among 2010 different m 5 C peaks, 830 methylated peaks in 782 genes were upregulated and 1,180 methylated peaks in 1,088 genes were downregulated in the aged hippocampi. Most of the m 5 C sites in the hippocampal transcriptome were distributed at the coding sequence, while the fewest m 5 C sites found in the 5′ untranslated regions (5′ UTRs). Young and aged mice showed a similar enrichment of the most credible motif. The protein level of the m 5 C demethylase TET2 was downregulated during aging, suggesting that TET2 may potentially influence neuronal health and even cognitive function through epigenetic mechanisms. Conclusions Our data demonstrated different m 5 C-enriched regions in the young and aged hippocampi, providing novel insight into the possible functions of m 5 C methylation in brain aging.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0077/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147882019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Luteolin alleviates lung cancer pain in mice by modulating AKT1 木犀草素通过调节AKT1减轻小鼠肺癌疼痛

Turkish Journal of Biochemistry Pub Date : 2025-12-22 DOI: 10.1515/tjb-2025-0263

Haiyan Tu, Shanshan Qi, Zhang Cl, Jie Yang

{"title":"Luteolin alleviates lung cancer pain in mice by modulating AKT1","authors":"Haiyan Tu, Shanshan Qi, Zhang Cl, Jie Yang","doi":"10.1515/tjb-2025-0263","DOIUrl":"https://doi.org/10.1515/tjb-2025-0263","url":null,"abstract":"Abstract Objetives The treatment of lung cancer pain (LCP) faces the double challenge of high side effects of analgesics and unclear mechanisms. Luteolin (LUT), an active ingredient of Salvia miltiorrhiza Bge., has anti-tumor potential, but its mechanism in alleviating LCP has not been elucidated completely. To elucidate the molecular mechanism of LUT in alleviating LCP by modulating the AKT1. Methods Based on the network pharmacology strategy, potential active ingredients of Salvia miltiorrhiza Bge. and their targets for the treatment of LCP were collected from the TCMSP, HERB, and CTD databases. A protein-protein interaction (PPI) network was constructed in the STRING database to identify the hub genes. Detection of AKT1 expression was performed by RT-qPCR or western blot. The degree of pain in lung cancer patients was quantified using the Numeric Rating Scale (NRS). The CCK-8 and Transwell assays were used to assess human lung carcinoma epithelial cell (A549) viability and invasiveness. The sensitivity to pain in bone metastasis mice was assessed by measuring the mechanical paw withdrawal threshold. Results AKT1 had the highest node degree value in the PPI network. The clinical analysis showed that AKT1 expression level was positively correlated with LCP. Cellular experiments showed that LUT concentration-dependently inhibited the cell viability of A549 cells and hindered cell invasion by down-regulating AKT1. The in vivo experiments showed that LUT treatment alleviated the pain of bone metastasis mice and decreased AKT1 expression. Conclusions LUT suppressed lung cancer cell invasion and relieved LCP through AKT1 inhibition.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0263/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147906354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MiR-101-3p alleviates TGF-β1-induced fibrosis of renal tubular epithelial cells by inhibiting EZH2 in chronic kidney disease MiR-101-3p通过抑制EZH2在慢性肾脏疾病中减轻TGF-β1诱导的肾小管上皮细胞纤维化

Turkish Journal of Biochemistry Pub Date : 2025-12-12 DOI: 10.1515/tjb-2025-0357

Li Xu, Xinsheng Xie, Yong Li, Peng Zhou, Wei An, Sun Danan, Xinxin Qu

{"title":"MiR-101-3p alleviates TGF-β1-induced fibrosis of renal tubular epithelial cells by inhibiting EZH2 in chronic kidney disease","authors":"Li Xu, Xinsheng Xie, Yong Li, Peng Zhou, Wei An, Sun Danan, Xinxin Qu","doi":"10.1515/tjb-2025-0357","DOIUrl":"https://doi.org/10.1515/tjb-2025-0357","url":null,"abstract":"Abstract Objectives Renal fibrosis (RF) is a critical pathway in the progression of chronic kidney disease (CKD) to end-stage kidney diseases. This study aimed to investigate the role of miR-101-3p in the progression of fibrosis in renal tubular epithelial cells (RTECs) and to elucidate the underlying molecular mechanisms. Methods An RF cell model was established by induction with transforming growth factor-β1 (TGF-β1). The expression levels of miR-101-3p and fibrosis-associated proteins were measured using quantitative real-time reverse transcription polymerase chain reaction. Cell migration ability was detected by Transwell assay. The potential target genes of miR-101-3p were predicted through bioinformatic analysis. The interaction between miR-101-3p and EZH2 was verified using the luciferase assay and RNA immunoprecipitation (RIP) assay. Results HK-2 cells treated with TGF-β1 showed downregulated expression of miR-101-3p. Overexpression of miR-101-3p reduced cell migration and decreased the production of fibronectin, collagen IV and α-smooth muscle actin (α-SMA). EZH2 was identified as a downstream target gene of miR-101-3p. The interaction between miR-101-3p and EZH2 was confirmed by luciferase assay and RIP assay. EZH2 was upregulated in TGF-β1-induced cells. Upregulation of EZH2 partially reversed the anti-fibrotic effects caused by miR-101-3p overexpression. Conclusions miR-101-3p alleviates TGF-β1-induced fibrosis in RTECs by inhibiting EZH2. This study provides new insights into the molecular mechanisms of RF and suggests potential therapeutic targets for CKD.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0357/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147917802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LINC01711 facilitated gastric carcinoma progression by sponging miR-140-3p LINC01711通过海绵miR-140-3p促进胃癌进展

Turkish Journal of Biochemistry Pub Date : 2025-12-08 DOI: 10.1515/tjb-2025-0204

Weikang Su, Jiahuan Wang, Yan-Hui Sun, Xiao-Xiao Wang, Cong Wu, Liping Liu

{"title":"LINC01711 facilitated gastric carcinoma progression by sponging miR-140-3p","authors":"Weikang Su, Jiahuan Wang, Yan-Hui Sun, Xiao-Xiao Wang, Cong Wu, Liping Liu","doi":"10.1515/tjb-2025-0204","DOIUrl":"https://doi.org/10.1515/tjb-2025-0204","url":null,"abstract":"Abstract Objectives Gastric carcinoma (GC) remains a high-mortality malignancy that needs efficient ways for the prognosis and therapy of the disease. LncRNAs are biomolecules that participate in cancer progression by regulating gene expression. This study thus investigated the role of lncRNA LINC01711 in GC progression and the underlying mechanisms. Methods GC tumor and normal tissues were collected from 150 GC patients. qRT-PCR was used to test the expression of biomolecules. LncBook, Miranda, and starBase databases were employed to explore miRNAs that interact with LINC01711. The association between the biomolecules was validated via a dual luciferase reporter assay. Biological functions of biomolecules in GC cells were measured by the Cell Counting Kit-8 (CCK-8) and the transwell migration and invasion assays. Results This study found an upregulation of LINC01711 in GC tumor tissues compared to normal tissues. The upregulation of LINC01711 was an indicator of adverse clinical outcomes in GC patients. The miRNA that interacted with LINC01711 in GC was hsa-miR-140-3p. There was a negative correlation between the expression levels of LINC01711 and hsa-miR-140-3p in both GC tumor tissues and cells. LINC01711 promoted GC tumor cell proliferation, migration, and invasion by sponging hsa-miR-140-3p. Conclusions LINC01711 might be an ideal prognostic marker and treatment target for GC. The upregulation of LINC01711 was a negative prognostic indicator for GC patients. LINC01711 facilitated GC tumor cell activities related to GC progression by sponging hsa-miR-140-3p.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0204/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147882520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of ADSC exosome-loaded sustained-release nanosphere gel on cartilage repair: a study using chondrosarcoma cell line SW1353 负载ADSC外泌体的缓释纳米球凝胶对软骨修复的影响：基于软骨肉瘤细胞系SW1353的研究

Turkish Journal of Biochemistry Pub Date : 2025-12-02 DOI: 10.1515/tjb-2025-0129

Yuyang Li, Beibei Wang, Li Hong, Shuping Wang, Yanwei Gao

{"title":"Effect of ADSC exosome-loaded sustained-release nanosphere gel on cartilage repair: a study using chondrosarcoma cell line SW1353","authors":"Yuyang Li, Beibei Wang, Li Hong, Shuping Wang, Yanwei Gao","doi":"10.1515/tjb-2025-0129","DOIUrl":"https://doi.org/10.1515/tjb-2025-0129","url":null,"abstract":"Abstract Objectives This study aims to explore the function of ADSCs-derived exosomes within a hyaluronic acid (HA) hydrogel on chondrocytes. Methods ADSCs-Exo were isolated and characterized through western blot analysis. An HA hydrogel encapsulating ADSCs-Exo (HA@ADSCs-Exo) was formulated. To simulate cartilage injury, an IL-1β-induced cell model was constructed. MTT assay, flow cytometry, ELISA, and RT-qPCR were used to detect the cell viability, apoptosis, as well as inflammatory factors, oxidative stress indexes, and the levels of degradation-related proteins and synthesis-related proteins in SW1353 chondrocytes. Results In comparison to IL-1β induction, the presence of HA@ADSCs-Exo improved cell viability and mitigated cell apoptosis. HA@ADSCs-Exo significantly restricted the production of TNF-α and IL-6 in the context of IL-1β stimulation. Moreover, the addition of HA@ADSCs-Exo inhibited the intracellular leakage of MDA and promoted the formation of SOD. Ultimately, HA@ADSCs-Exo effectively suppressed the expression of chondrocyte degradation markers (MMP-13 and ADAMTS-1), while simultaneously facilitating the upregulation of chondrocyte reconstruction marker (Aggrecan). Conclusions HA@ADSCs-Exo demonstrates remarkable efficacy in mitigating chondrocyte damage induced by IL-1β. This innovative drug delivery system, which intricately combines HA-hydrogels with exosomes derived from ADSCs, offers a novel approach to addressing cartilage injury and has exhibited promising potential for facilitating cartilage repair.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"51 2","pages":"200-209"},"PeriodicalIF":0.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0129/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147912992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Xanthohumol inhibits extracellular matrix degradation via the Nrf2/PERK/ATF4/C/EBPβ pathway in osteoarthritis 黄腐酚通过Nrf2/PERK/ATF4/C/EBPβ途径抑制骨关节炎的细胞外基质降解

Turkish Journal of Biochemistry Pub Date : 2025-12-01 DOI: 10.1515/tjb-2025-0018

Tiansheng Zheng, Shuyi Niu, Qingluo Zhou, Jishang Huang, Jun Yi, Runhong Mei, Xuefeng Yu

{"title":"Xanthohumol inhibits extracellular matrix degradation via the Nrf2/PERK/ATF4/C/EBPβ pathway in osteoarthritis","authors":"Tiansheng Zheng, Shuyi Niu, Qingluo Zhou, Jishang Huang, Jun Yi, Runhong Mei, Xuefeng Yu","doi":"10.1515/tjb-2025-0018","DOIUrl":"https://doi.org/10.1515/tjb-2025-0018","url":null,"abstract":"Abstract Objectives This study aims to explore the therapeutic potential of Xanthohumol (XH) in mitigating osteoarthritis (OA) progression by inhibiting extracellular matrix (ECM) degradation. Specifically, it investigates the role of XH in reducing matrix metalloprotease-13 (MMP-13) activity and modulating the PRKR-like endoplasmic reticulum kinase/activating transcription factor 4 (PERK/ATF4) pathway while enhancing nuclear factor-erythroid 2-related factor 2 (Nrf2) activity. Methods In vitro experiments were conducted on OA chondrocytes (CTs) to evaluate MMP-13 production and collagen II expression following XH treatment. In vivo , XH was administered intraperitoneally, and cartilage degradation was assessed. Molecular analysis examined the expression of C/EBPβ, a downstream effector of the PERK/ATF4 pathway, and Nrf2 activity. Overexpression and knockdown experiments were performed to elucidate XH’s mechanistic effects. Results XH treatment reduced MMP-13 production by 46 % and increased collagen II expression by 38 % in vitro . In vivo , XH administration resulted in a 31 % decrease in cartilage degradation scores compared to controls. Mechanistically, XH decreased C/EBPβ expression and increased Nrf2 activity by 52 %. Overexpression of C/EBPβ or activation of the PERK/ATF4 pathway nullified XH’s protective effects, while Nrf2 knockdown abolished its benefits. Conclusions XH inhibits ECM degradation in OA by suppressing the PERK/ATF4/C/EBPβ pathway and activating Nrf2, demonstrating its potential as a low-cytotoxicity therapeutic agent for OA treatment. This approach offers a promising strategy for mitigating cartilage damage and advancing OA management.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"50 6","pages":"931-946"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0018/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147888811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0