Cytokine最新文献

{"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}

{"title":"Shedding new light on BACE1-mediated modulation of IL-6 signaling: Implications for neural activity and synaptic plasticity in mice","authors":"Buket Ucar Franke ,&nbsp;Kai Kummer ,&nbsp;Stefan Rose-John ,&nbsp;Stefan F. Lichtenthaler ,&nbsp;Michaela Kress","doi":"10.1016/j.cyto.2025.156925","DOIUrl":"10.1016/j.cyto.2025.156925","url":null,"abstract":"<div><div>The pleiotropic cytokine IL-6 regulates numerous processes in the body, including neuronal functions. IL-6 either binds to membrane-bound receptor (mIL-6R) and triggers signaling via heteromerization with the signal transducer gp130 (classical signaling), or binds to its soluble form (sIL-6R) to act on cells that do not express mIL-6R (trans-signaling). The ß-secretase BACE1 can cleave gp130 as well as IL-6R and we hypothesized that BACE1 may alter neuron activity and synaptic transmission via modulation of IL-6 signaling.</div><div>We used multielectrode array (MEA) recordings to monitor electrical activity of neuronal networks in acute cerebellar slices as well as long-term potentiation (LTP) induced by high-frequency stimulation in the hippocampus and to assess how exposure to IL-6 affects these processes. A pharmacological approach was applied to elucidate the contribution of trans-signaling involving BACE1.</div><div>Spontaneous neuronal activity in cerebellar slices significantly decreased upon perfusion with IL-6 but not LIF and recovered during wash out. BACE1 inhibitors verubecestat or AZD3839 abolished the inhibitory effects of IL-6. Furthermore, IL-6 and LIF reversibly inhibited LTP in hippocampal slices, and in contrast to cerebellar neurons, BACE1 inhibitors verubecestat or AZD3839 did not abolish the inhibitory effect of IL-6 on LTP. Interestingly, a dramatic rebound effect on excitatory postsynaptic potentials was observed with BACE1 inhibitor AZD3839 but not verubecestat during wash out.</div><div>Our results support relevant and differential roles of IL-6, LIF and BACE1 in pathways modulating neuronal discharge activity in the cerebellum and the synaptic plasticity in the hippocampus, and a possible involvement of this interaction in deficits of memory and learning.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156925"},"PeriodicalIF":3.7,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761167","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":"Exploring the genetic association between inflammatory cytokines and primary ovarian insufficiency: A Mendelian randomization study","authors":"Jie Wu ,&nbsp;Yancheng Fu ,&nbsp;Zhengqi Qiu","doi":"10.1016/j.cyto.2025.156937","DOIUrl":"10.1016/j.cyto.2025.156937","url":null,"abstract":"<div><div><strong>Purpose:</strong> This study aims to investigate the genetic underpinnings of Primary Ovarian Insufficiency (POI) by examining the association between 91 inflammatory cytokines identified through genome-wide association studies (GWAS) and POI, using Mendelian randomization (MR) to explore potential causal relationships.</div><div><strong>Methods:</strong> We utilized Mendelian Randomization (MR) to investigate the causative links between inflammatory cytokines and POI, selecting genetic variants associated with cytokine levels as instrumental variables.</div><div><strong>Results:</strong> Utilizing the Inverse Variance Weighted (IVW) method, our Mendelian Randomization (MR) study elucidated the influence of inflammatory cytokines on POI. We discovered that certain cytokines exhibit a protective association: C<img>C motif chemokine 19 (CCL19) [OR 0.58; 95 % CI: 0.36–0.93; <em>p</em> = 0.024], Interleukin-10 (IL-10) [OR 0.41; 95 % CI: 0.23–0.72; <em>p</em> = 0.002], Interleukin-17 A (IL-17 A) [OR 0.44; 95 % CI: 0.20–0.96; <em>p</em> = 0.040], and Monocyte chemotactic protein 3 (MCP-3) [OR 0.51; 95 % CI: 0.29–0.89; <em>p</em> = 0.018]. Conversely, an elevated level of interleukin-33 in blood plasma was identified as a risk factor for POI [OR 2.83; 95 % CI: 1.23–6.50; <em>p</em> = 0.015].</div><div><strong>Conclusion:</strong> Our findings indicate a significant correlation between specific inflammatory cytokines and the risk of developing POI. The negative association of cytokines such as CCL19, IL-10, IL-17 A, and MCP-3 suggests a protective effect against POI, whereas the positive association of IL-33 levels implies a potential adverse impact. These insights could guide future research towards targeted immunomodulatory therapies for the management and prevention of POI.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156937"},"PeriodicalIF":3.7,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761170","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":"Effects of botulinum toxin type a on nucleotide binding oligomerization domain-like receptor 3 inflammasome in trigeminal ganglion of a rat migraine model","authors":"Jun Shen ,&nbsp;Xiaofeng Zhu ,&nbsp;Lei Xia ,&nbsp;Jin Shang ,&nbsp;Ming Wei ,&nbsp;Qiu Han","doi":"10.1016/j.cyto.2025.156934","DOIUrl":"10.1016/j.cyto.2025.156934","url":null,"abstract":"<div><h3>Background</h3><div>Botulinum toxin type A (BTX-A) has been used in the prevention and treatment of chronic migraine, but the detailed mechanism was not clear completely.</div></div><div><h3>Objective</h3><div>The effects of BTX-A on nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome and interleukin-1 beta (IL-1β) were explored in the trigeminal ganglion of migraine model rats.</div></div><div><h3>Methods</h3><div>Healthy adult male Sprague-Dawley (SD) rats were randomly divided into groups. Von Frey fiber filaments were used to detect the periorbital pain area of rats. The immunoblotting and Immunofluorescence were used to detect the expression of NLRP3 inflammasome and IL-1β in the trigeminal ganglia of rats.</div></div><div><h3>Results</h3><div>The periorbital pain area of rats in the migraine model group was significantly lower than that of the Sham group, and the difference was statistically significant (<em>p</em> &lt; 0.05). Compared with the Sham group, the expressions of NLRP3, pro-caspase-1, caspase-1 and mature IL-1β in the migraine model group were significantly increased, and the difference was statistically significant (<em>p</em> &lt; 0.05). Compared with the IA control group, the expressions of NLRP3, pro-caspase-1, caspase-1 and mature IL-1β in 5 U/kg BTX and 10 U/kg BTX-A group were significantly reduced (<em>p</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>BTX-A inhibits the synthesis of NLRP3 inflammasome and mature IL-1β in the trigeminal ganglion from rat migraine models. Its inhibitory effect on the inflammation of the primary nociceptive neurons of the trigeminal nerve may be one of its important mechanisms for the prevention of migraine.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156934"},"PeriodicalIF":3.7,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761166","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 role of TNF in metabolic disorders and liver diseases","authors":"Chuze Xu ,&nbsp;Sohaib Hasan Abdullah Ezzi ,&nbsp;Xiaodi Zou ,&nbsp;Yanzhao Dong ,&nbsp;Ahmad Alhaskawi ,&nbsp;Haiying Zhou ,&nbsp;Vishnu Goutham Kota ,&nbsp;Mohamed Hasan Abdulla Hasan Abdulla ,&nbsp;Sahar Ahmed Abdalbary ,&nbsp;Hui Lu","doi":"10.1016/j.cyto.2025.156933","DOIUrl":"10.1016/j.cyto.2025.156933","url":null,"abstract":"<div><div>Tumor necrosis factor (TNF) is identified as a pro-inflammatory cytokine critical to the pathology of liver disease. In the carbohydrate metabolism, TNF has been demonstrated to impede the insulin signaling pathway, thereby precipitating glucose intolerance and insulin resistance. In lipid metabolism, TNF upregulates genes implicated in fatty acid synthesis, resulting in increased lipid accumulation within the liver. In amino acid metabolism, TNF has shown to promote the gene expression for amino acid catabolism, leading to decreased protein synthesis. Additionally, TNF stimulates the production of other chemokines and inflammatory cytokines that can further exacerbate liver injury. Overall, TNF is crucial in developing liver diseases by disrupting various metabolic pathways in the liver, causing insulin resistance, lipid accumulation, and decreased protein synthesis. This review summarizes the present understanding of TNF's role in the regulation of carbohydrate, lipid and amino acid metabolism in liver disease together with its potential therapeutic implications.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156933"},"PeriodicalIF":3.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143747949","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}