Cytokine最新文献

{"title":"Genetic insights into neuroblastoma: the role of immune cell features","authors":"Yunfei Ma ,&nbsp;Qiang He ,&nbsp;Yan Su ,&nbsp;Wen Zhao ,&nbsp;Cheng Huang ,&nbsp;Jing Qin ,&nbsp;Shengjie You ,&nbsp;Yan Hu ,&nbsp;Xin Ni","doi":"10.1016/j.cyto.2025.156942","DOIUrl":"10.1016/j.cyto.2025.156942","url":null,"abstract":"<div><h3>Objective</h3><div>To elucidate the causal relationship between immune cells and neuroblastoma, we conducted a two-sample Mendelian randomization (MR) analysis.</div></div><div><h3>Materials and methods</h3><div>The exposure and outcome data for the genome-wide association study (GWAS) used in this research were sourced from an open-access database. The study utilized two-sample MR analysis to evaluate the causal relationship between 731 immune cell features and neuroblastoma. The main approach to explore this relationship is to apply the inverse variance weighting (IVW) method. In addition, sensitivity analyses including leave-one-out analysis, Cochran's Q test, Mendelian randomization Egger method (MR-Egger) intercept test and Mendelian randomization pleiotropy residual sum and outlier test (MR-PRESSO) were performed to verify the reliability of the MR results.</div></div><div><h3>Results</h3><div>The study identifies five immune cell traits as causally contributing to neuroblastoma risk, including CD3⁻ lymphocyte (% of leukocytes) (IVW: OR[95 % CI] 0.65[0.42–0.99], <em>P</em> = 0.0469), CD86 on granulocyte (IVW: OR[95 % CI] 0.61[0.41–0.92], <em>P</em> = 0.0167), FSC-A on granulocyte(IVW: OR[95 % CI] 0.73[0.57–0.93], <em>P</em> = 0.0117), HLA DR+ CD8+ T cell Absolute Count(IVW: OR[95 % CI]: 1.38[1.01–1.88], <em>P</em> = 0.0408), IgD− CD38+ B cell Absolute Count(IVW: OR[95 % CI] 0.42[0.27–0.66], <em>P</em> = 0.0002). The results of sensitivity analyses were consistent with the main findings.</div></div><div><h3>Conclusion</h3><div>We demonstrated a close causal relationship between specific types of immune cells and neuroblastoma by genetic methods, offering valuable guidance for future clinical studies.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156942"},"PeriodicalIF":3.7,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of GFPT2 enhances cisplatin chemotherapy sensitivity in STK11/KRAS mutant non-small cell lung cancer by regulating the hexosamine biosynthesis pathway, resisting tumor growth","authors":"Cheng Zhang ,&nbsp;Xuelei Yin ,&nbsp;Jun Jiang ,&nbsp;Peng Wang ,&nbsp;Yirong Wang","doi":"10.1016/j.cyto.2025.156943","DOIUrl":"10.1016/j.cyto.2025.156943","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the role of GFPT2 in the sensitivity of STK11/KRAS lung cancer cells to cisplatin chemotherapy, and its underlying mechanism.</div></div><div><h3>Materials &amp; methods</h3><div>A549 and H460 cells were used to analyze the effect of GFPT2 on cisplatin chemotherapy sensitivity, as both carry KRAS mutations and H460 has LKB1 inactivation mutations, meeting the requirements of a KRAS/LKB1 co mutant tumor model. The levels of UDP-GlcNAc, OGT, OGA, and O-GlcNAc in the HBP pathway were also determined. To verify the potential role of HBP, we added OGT inhibitors. In vivo, we constructed a nude mouse model bearing A549 tumor to further validate the results of in vitro cell experiments.</div></div><div><h3>Results</h3><div>GFPT2 silencing can significantly inhibit cell proliferation, invasion, and migration, promote cell apoptosis, and enhance the effect of cisplatin (<em>p</em> &lt; 0.05). After OSMI-1 processing, GFPT2 enhances O-GlcNAc modification levels via the OGT-mediated HBP, thereby decreasing the sensitivity of STK11/KRAS mutant cells to cisplatin chemotherapy. In addition, GFPT2 silencing enhances the chemotherapy sensitivity of cisplatin and inhibits tumor growth, while overexpression of GFPT2 weakens this effect (<em>p</em> &lt; 0.05). The above results provide new targets and combination therapy options for the clinical treatment of KRAS/LKB1 mutant lung cancer.</div></div><div><h3>Conclusion</h3><div>Our study found that inhibiting GFPT2 can enhance the chemotherapy sensitivity of cisplatin to STK11/KRAS/LKB1 mutant NSCLCs cells through the OGT mediated HBP pathway, filling a key gap in the chemotherapy resistance mechanism of KRAS/LKB1 mutant lung cancer.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156943"},"PeriodicalIF":3.7,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00426 promotes the progression of atherosclerosis by regulating miR-873-5p/SRRM2 axis","authors":"Bo Zhou ,&nbsp;Lu Gan ,&nbsp;Pimo Zhou ,&nbsp;Tai Yang ,&nbsp;Fang Tang ,&nbsp;Peng Jin ,&nbsp;Ping Jin ,&nbsp;Jiulin Chen","doi":"10.1016/j.cyto.2025.156938","DOIUrl":"10.1016/j.cyto.2025.156938","url":null,"abstract":"<div><h3>Background</h3><div>Atherosclerosis (AS) is a disease that occurs in the great arteries and is the main cause of cardiovascular disease and death.</div></div><div><h3>Objective</h3><div>To investigate the clinical significance of LINC00426 in AS and to investigate that LINC00426 regulates PDGF-BB-induced proliferation, migration, invasion and inflammatory response of vascular smooth muscle cells (VSMCs) by modulating miR-873-5p/SRRM2 axis.</div></div><div><h3>Methods</h3><div>The expression of LINC00426 was detected using RT-qPCR. The diagnostic role of LINC00426 in AS was analyzed with ROC curves. CCK-8 assay was used to measure cell proliferation, and transwell assay was used to measure cell migration and invasion ability. The targeted binding relationship between LINC00426 and miR-873-5p, miR-873-5p and SRRM2 was detected using dual-luciferase reporter gene assay. The concentration of proinflammatory factors was detected by using ELISA kit.</div></div><div><h3>Result</h3><div>The expression of LINC00426 was increased in patients with AS, and LINC00426 had a diagnostic role in AS. In addition, LINC00426 regulated PDGF-BB-induced proliferation, migration, invasion, and inflammation of VSMCs by regulating miR-873-5p/SRRM2 axis.</div></div><div><h3>Conclusion</h3><div>LINC00426 may function as a biomarker for the diagnosis and treatment of AS.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156938"},"PeriodicalIF":3.7,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143829460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotinamide metabolism affects the prognosis of hepatocellular carcinoma by influencing the tumor microenvironment","authors":"Min Zhou ,&nbsp;Wenhui Zhao ,&nbsp;Xiaobo Zhang ,&nbsp;Ye Cheng ,&nbsp;Mengxiang Wang ,&nbsp;Yan Chen ,&nbsp;Lingrui Zhao","doi":"10.1016/j.cyto.2025.156939","DOIUrl":"10.1016/j.cyto.2025.156939","url":null,"abstract":"<div><div>In this study, we utilized the public database along with single-cell genomics techniques to systematically analyze the expression patterns and clinical significance of key genes in the nicotinamide metabolism pathway in liver cancer samples. The findings indicate that differential nicotinamide metabolism-related key genes are expressed in liver cancer samples. The liver cancer samples were put into separate subgroups using consistency clustering analysis based on differential gene expression levels observed. Additionally, immune infiltration and drug sensitivity analysis also revealed differences between the two subgroups. Survival analysis suggested that the key genes were associated with prognosis. Finally, a prognostic model was established using the key genes, offering a fresh viewpoint on the molecular mechanism investigating liver cancer. This study demonstrated the significant correlation between key genes in the nicotinamide metabolism pathway and the occurrence and progression of liver cancer and indicated that these key genes could serve as prognostic markers and tailored treatment targets for liver cancer.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156939"},"PeriodicalIF":3.7,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ADAM17/ACE2 interaction mediates cadmium-induced brain damage and neuroinflammation in Wistar rats","authors":"Ahmed A. Morsi ,&nbsp;Ezat A. Mersal ,&nbsp;Marwa Omar Abdel All ,&nbsp;Alshaymaa M. Abdelmenem ,&nbsp;Amal F. Dawood ,&nbsp;Atheer Alanazi ,&nbsp;Norah Mahdi ,&nbsp;Mohamed S. Salim","doi":"10.1016/j.cyto.2025.156936","DOIUrl":"10.1016/j.cyto.2025.156936","url":null,"abstract":"<div><div>Angiotensin-converting enzyme 2 (ACE2) is a critical component in the renin-angiotensin system. A Disintegrin And Metalloprotease 17 (ADAM17) is the first identified sheddase for common inflammatory cytokines. Changes in ACE2 expression and its biological activity facilitated by ADAM17 are involved in several diseases including neurodegenerative disorders. Herein, the study investigated an innovative viewpoint on cadmium (Cd)-induced neurotoxicity and explored whether ADAM17/ACE2 interplay mediated the Cd-induced brain injury and neuroinflammation. For this aim, 32 adult male Wistar rats were included and randomly grouped. Eight rats served as a control group and the remaining 24 experimental rats were exposed to Cd (5 mg/kg/day, orally, 21 days); assigned as either Cd-alone (Cd group), received ADAM17 inhibitor [TAPI-1, 10 mg/kg, intraperitoneal] (Cd/TAPI-1 group), or received vitamin E, 100 mg/kg/d, orally (Cd/vit E group). Ultimately, the brains were harvested and exposed to biochemical, histological, and immunohistochemical (IHC) studies for measuring oxidative stress and inflammatory markers, histopathological examination, and for IHC identification of ADAM17, ACE2, and glial fibrillary acidic protein (GFAP). Cd resulted in biochemical disturbances in the inflammatory and oxidative stress markers, degenerative histopathological changes in the cerebral cortex and hippocampus, and enhanced ADAM17 and GFAP expression, meanwhile downregulated ACE2 expression. Vitamin E showed a superior effect in maintaining the oxidative/antioxidant-balanced defense system. However, the biochemical and histological changes in the brain were more effectively alleviated by TAPI-1 administration than by the partial improvement made by vitamin E therapy. These observations suggested that oxidative stress was involved in Cd-mediated upregulation of ADAM17 and ACE2 shedding. It was concluded that oxidative stress, at least in part, resulted in ADAM17-mediated ACE2 cleavage in the current Cd-induced brain damage.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156936"},"PeriodicalIF":3.7,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143790936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A thorough analysis of data on the correlation between IL-16 polymorphisms and the susceptibility to knee osteoarthritis: A meta-analysis","authors":"Amirhossein Omidi ,&nbsp;Mohammad Bahrami ,&nbsp;Seyed Alireza Dastgheib ,&nbsp;Ahmadreza Golshan-Tafti ,&nbsp;Ali Masoudi ,&nbsp;Amirmasoud Shiri ,&nbsp;Maryam Aghasipour ,&nbsp;Amirhossein Shahbazi ,&nbsp;Kazem Aghili ,&nbsp;Hossein Neamatzadeh","doi":"10.1016/j.cyto.2025.156929","DOIUrl":"10.1016/j.cyto.2025.156929","url":null,"abstract":"<div><h3>Background</h3><div>Knee osteoarthritis (KOA) is a multifactorial condition affected by genetic and environmental factors. Studies have explored the relationship between IL-16 genetic polymorphisms and KOA risk, but findings have been inconclusive. This meta-analysis seeks to assess the association between IL-16 polymorphisms and KOA risk.</div></div><div><h3>Methods</h3><div>A systematic literature search was conducted in several databases, including PubMed, Web of Science, EMBASE, SciELO, and CNKI, for studies published until June 1, 2024. Two independent researchers identified peer-reviewed articles in English, Portuguese, and Chinese using keywords related to “Knee Osteoarthritis” and “Interleukin 16.” Relevant references were also manually reviewed for additional studies. Pooled odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated to assess the association strength. Additionally, minor allele frequencies (MAFs), Hardy-Weinberg equilibrium (HWE) data, heterogeneity, publication bias, and Newcastle-Ottawa scores (NOS) were evaluated.</div></div><div><h3>Results</h3><div>This analysis included 15 case-control studies, encompassing 1747 individuals with KOA and 1627 healthy controls. Within these studies, five investigated the genetic variations rs11556218 (584 cases, 542 controls), rs4778889 (583 cases, 543 controls), and rs4072111 (580 cases, 542 controls). The findings suggest that the IL-16 variants rs11556218 and rs4072111 may offer protection against KOA development, while no link exists between the rs4778889 variant and KOA susceptibility. The variability in IL-16 polymorphisms, particularly in Asian and Chinese populations, indicates different genetic associations with KOA risk. Strong results, supported by sensitivity analyses and the absence of significant publication bias, emphasize the influence of study methods on the relationship between these polymorphisms and KOA risk.</div></div><div><h3>Conclusions</h3><div>The analysis of three polymorphisms—rs11556218, rs4778889, and rs4072111—shows varying associations with KOA. Rs11556218 and rs4072111 offer protective effects in non-Asian populations, while rs4778889 shows no significant association across cohorts. Notably, rs11556218 and rs4072111 do not correlate with KOA susceptibility in Asian and Chinese populations, suggesting ethnic differences in genetic influences on KOA.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143784966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol interrupts Wnt/β-catenin signalling in cervical cancer by activating ten-eleven translocation 5-methylcytosine dioxygenase 1","authors":"Ji Ren ,&nbsp;Luhong Xie ,&nbsp;Xiaoyu Zhu ,&nbsp;Xiuying Chen ,&nbsp;Lin Wei ,&nbsp;Dianqin Xu ,&nbsp;Kun Qiao ,&nbsp;Shaoju Min ,&nbsp;Yan Ding ,&nbsp;Yujie Tan","doi":"10.1016/j.cyto.2025.156930","DOIUrl":"10.1016/j.cyto.2025.156930","url":null,"abstract":"<div><div>Epigenetic modification can be a key weapon employed by both sides of the battle between Cervical Cancer progression due to persistent high-risk papillomavirus (hr-HPV) infection and the development of anti-cancer modalities. Alongside the overactivated Wnt/β-catenin activity, reduced TET1 expression and ratio of 5-hydroxymethylcytosine (5hmC) to 5-methylcytosine (5mC) were found in cervical cancer, which was correlated with lymph node metastasis. After treating cervical cancer cells with Resveratrol (RES), we found that TET1 expression was elevated and Wnt/β-catenin pathway activity was suppressed. Therefore, the aim of this study is to investigate the influence of resveratrol on the TET1 and Wnt/β-catenin pathways, and to elucidate the molecular mechanisms involved in this process, thereby clarifying the potential value of RES in the treatment of cervical cancer. Our data illustrate the TET1-mediated epigenetic modulation was an integral part of the effects of RES on the Wnt/β-catenin pathway in cervical cancer.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156930"},"PeriodicalIF":3.7,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel genetic associations with childhood adipocytokines in Indian adolescents","authors":"Janaki M. Nair ,&nbsp;Ganesh Chauhan ,&nbsp;Gauri Prasad ,&nbsp;Shraddha Chakraborty ,&nbsp;Khushdeep Bandesh ,&nbsp;Anil K. Giri ,&nbsp;Raman K. Marwaha ,&nbsp;Analabha Basu ,&nbsp;Nikhil Tandon ,&nbsp;Dwaipayan Bharadwaj","doi":"10.1016/j.cyto.2025.156935","DOIUrl":"10.1016/j.cyto.2025.156935","url":null,"abstract":"<div><div>Adipocytokines, including leptin, adiponectin, and resistin, are key mediators linking adiposity, insulin resistance, and inflammation. We present the first genome-wide association study (GWAS; <em>N</em> = 5258) and exome-wide association study (ExWAS; <em>N</em> = 4578) on leptin, adiponectin, and resistin in South Asian population. We identified novel associations in genes <em>ZNF467</em>, and <em>LEPREL2</em> for leptin; <em>ZNF467, LEPREL2, CRLF3, ZNF732, SOX30, XIRP1, ATP8B3, SPATA2L, TMCO4, TLN2, ABCA12</em>, and <em>SHB</em> for adiponectin; and <em>D2HGDH</em> for resistin. Additionally, we confirmed known associations of <em>FTO, MC4R</em>, and <em>HOXB3</em> with leptin and <em>ADIPOQ</em> with adiponectin. Notably, <em>ADIPOQ</em> variants were consistently significant across GWAS, ExWAS, and gene-based analyses, reinforcing their central role in regulating adiponectin levels. Most of these novel associations identified were population-specific, highlighting the importance of studying diverse populations to uncover unique genetic signals. After adjusting for BMI, the associations with adiponectin and resistin remained significant, whereas most associations for leptin weakened in both effect size and significance. Functional annotation revealed that the identified variants were enriched for expression in adipose tissue, the brain (cerebellar hemisphere and cerebral cortex), and the pituitary gland. These variants act as eQTLs and splice-QTLs in adipose, brain, and pancreas, suggesting cross-tissue regulatory mechanisms. ExWAS further implicated rare variant burden in genes such as <em>LONP1, ZNF335,</em> and <em>TTC16</em> for adiponectin and resistin. These findings enhance our understanding of adipocytokine biology, emphasises the need for population-specific genetic research, and lays foundation for future functional studies.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156935"},"PeriodicalIF":3.7,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrogen combined with needle-embedding therapy alleviates traumatic brain injury by inhibiting NLRP3 inflammasome activation via STING signaling pathway","authors":"Fan Wu ,&nbsp;Wenting Su ,&nbsp;Xin Wang ,&nbsp;Chenhui Wang ,&nbsp;Yongxing Sun ,&nbsp;Baoguo Wang","doi":"10.1016/j.cyto.2025.156931","DOIUrl":"10.1016/j.cyto.2025.156931","url":null,"abstract":"<div><h3>Background</h3><div>Traumatic brain injury (TBI) is a primary cause of disability and death worldwide and with unmet effective therapies. Molecular hydrogen (H₂) exerts latent therapeutic means for TBI. Nevertheless, few studies have illustrated the roles of hydrogen combined with needle-embedding therapy (H₂ + NET) in TBI and its exact mechanism remains unclear. Here, we elucidated the underlying mechanisms of H₂ + NET in the TBI progression.</div></div><div><h3>Methods</h3><div>Controlled cortical impact (CCI) method was conducted to construct TBI mouse model. The mNSS test was used for neurological function measurement. Nissl staining for evaluating neuronal injury, TUNEL assay for determining neuronal apoptosis and ELISA assay was applied for adenosine, ATP level and inflammatory cytokines determination. The relative mRNA levels of inflammatory elements were assessed by qRT-PCR analysis. Iba-1, NLRP3 and STING expression were determined through immunofluorescence staining. The expression of NLRP3 inflammasome related proteins and STING signaling pathway associated proteins were evaluated using Western blot.</div></div><div><h3>Results</h3><div>H₂ or NET treatment mitigated brain injury and reduced brain water content in CCI-induced TBI mouse model. CCI induction promoted microglia activation and inflammatory response, thereby activating the NLRP3 inflammasome activity and STING signaling pathway, which was partly reversed by H₂ or NET treatment. However, H₂ + NET significantly ameliorated brain oedema, and further inhibited inflammatory response, NLRP3 inflammasome activation and STING pathway activation in TBI mice when compared to the H₂ or NET alone treatment group.</div></div><div><h3>Conclusion</h3><div>Hydrogen combined with needle-embedding therapy acts as a promising intervention method for TBI through inhibiting NLRP3 inflammasome activation via STING signaling pathway.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156931"},"PeriodicalIF":3.7,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143767689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The synergistic effects of prostaglandin and IL-1β on myometrial and cervical stromal cells at the onset of labor","authors":"Qian Huang,&nbsp;Pin Li,&nbsp;Zheng Zheng,&nbsp;Xiaoyan Sha,&nbsp;Lele Wang,&nbsp;Baohua Lin,&nbsp;Junjie Bao,&nbsp;Yanmin Jiang ,&nbsp;Huishu Liu","doi":"10.1016/j.cyto.2025.156927","DOIUrl":"10.1016/j.cyto.2025.156927","url":null,"abstract":"<div><div>Inflammatory cytokines such as IL-1β and prostaglandins (PGs) are pivotal in the initiation of labor. Nevertheless, the synergistic interaction between PGs and IL-1β remains to be fully elucidated. Labor is defined as regular and gradually increasing uterine contractions accompanied by progressive dilation of the cervix, and descent of the fetal. This study employed Luminex to monitor alterations in inflammatory cytokine levels within myometrial tissue (<em>n</em> = 10) during labor compared to non-labor (n = 10) conditions. And the synergistic relationship between PGs and IL-1β by investigating the primary myometrium cells and cervical stromal cells culture. The results showed that the inflammatory cytokines of IL-1β, IL-6, IL-8 and TNF-α in the myometrium tissue were increased in labor group. In myometrium cells, PGF2α and IL-1β synergistically up-regulated <em>COX</em>-2 mRNA, upregulated the transcription of PRA and PRB, PGF2α alleviated that IL-1β up-regulated <em>IL-8</em> mRNA. In cervical stromal cells, IL-1β up-regulated the COX-2 and PRB protein expression. PGE2 abated that IL-1β up-regulated <em>IL-8</em> mRNA. PGE increased the expression of PRs, which is more pronounced with the prolonged duration. Ratio of PRA/PRB show an increased trend with IL-1β and PGE2 co-regulated. This study further clarified the synergistic regulatory mechanism of IL-1β and PGs, offering a theoretical foundation for the development of strategies aimed at labor induction and the prevention and treatment of preterm birth.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156927"},"PeriodicalIF":3.7,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}