Hyun Young Park, Soo Hyun Choi, JaeSang Ko, Jin Sook Yoon
{"title":"Therapeutic effect of nintedanib in orbital fibroblasts in patients with Graves' orbitopathy.","authors":"Hyun Young Park, Soo Hyun Choi, JaeSang Ko, Jin Sook Yoon","doi":"10.1080/08923973.2025.2491554","DOIUrl":"10.1080/08923973.2025.2491554","url":null,"abstract":"<p><strong>Background: </strong>Nintedanib is a potent antifibrotic angiokinase inhibitor approved for various fibrotic lung diseases. Potential therapeutic efficacy of nintedanib in various inflammatory diseases is under investigation. In this study, we investigated the therapeutic effect of nintedanib on adipogenesis and fibrosis in orbital fibroblasts in patients with Graves' orbitopathy (GO).</p><p><strong>Methods: </strong>Primary orbital fibroblasts were cultured from orbital connective tissue of patients with GO and healthy controls. The cells were pretreated with nintedanib before stimulation with either interleukin (IL)-1β, transforming growth factor (TGF)-β, insulin-like growth factor-1, or IL-11. Fibrosis-related and intracellular signaling protein expressions were assessed using western blotting. Hyaluronan and procollagen concentrations were quantified using enzyme-linked immunosorbent assay. Adipogenesis was quantified by Oil Red O staining and the levels of adipogenic transcription factors were determined by Western blot.</p><p><strong>Results: </strong>TGF-β-induced fibronectin and collagen 1/3 protein expression was abrogated by nintedanib treatment. Nintedanib decreased the phosphorylation of signal transducer and activator of transcription 3, SMAD 2/3, Akt, c-Jun N-terminal kinase, and extracellular regulated protein kinase. Exposure to nintedanib hindered adipocyte differentiation and expression of adipogenic transcription factors, including peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding protein α/β, adipocyte protein 2, adiponectin, and leptin. Additionally, nintedanib reduced hyaluronan and procollagen secretion.</p><p><strong>Conclusions: </strong>Nintedanib suppressed profibrotic protein production, adipogenesis, and hyaluronan production in <i>in vitro</i>. These findings indicate the potential therapeutic efficacy of nintedanib in GO management.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"406-418"},"PeriodicalIF":2.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of infliximab infusion on clinical symptom scores and serum cytokines in patients with inflammatory bowel disease.","authors":"Wei Tan, Hao Wang, Hong Guo","doi":"10.1080/08923973.2025.2504908","DOIUrl":"10.1080/08923973.2025.2504908","url":null,"abstract":"<p><strong>Background: </strong>Inflammatory bowel disease (IBD) is a chronic relapsing gastrointestinal disorder. Infliximab (INF) has shown good efficacy in IBD treatment, but its specific impact requires further exploration. This study aimed to assess the effects of intravenous INF on clinical symptom scores and serum cytokine levels in IBD patients.</p><p><strong>Methods: </strong>A retrospective review of 126 IBD patients treated with INF was conducted. Baseline data, Mayo scores, Crohn's Disease Activity Index (CDAI) scores at 6 and 12 months, and serum levels of TNF-α, IL-6, IL-10, and CRP were recorded. Correlations between disease activity scores and inflammatory markers were analyzed, and the relationship between baseline indicators and treatment efficacy was examined.</p><p><strong>Results: </strong>At 12 months, Mayo and CDAI scores, TNF-α, IL-6, and CRP levels were significantly reduced, while IL-10 levels increased. Disease activity scores positively correlated with TNF-α, IL-6, and IL-1β, and negatively with IL-10. Factors such as Crohn's disease subtype, age, high baseline CDAI or Mayo scores, elevated TNF-α, IL-6, CRP, and longer disease duration were associated with poorer outcomes (<i>p</i> < 0.05). Multivariate analysis identified disease type, high baseline disease activity, long disease duration, and elevated inflammatory markers as independent risk factors. Adverse reactions were infrequent, with no serious adverse events reported.</p><p><strong>Conclusion: </strong>Intravenous INF effectively improves clinical symptoms and modulates inflammatory cytokines in IBD patients, with favorable safety and increasing efficacy over time. However, the limited sample size and lack of long-term data warrant further validation in larger, prospective multicenter studies.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"419-428"},"PeriodicalIF":2.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mai Chen, Pengchao Ma, Jingxing Liang, Shunming Zhu, Juan Ren
{"title":"Fenofibrate ameliorates LPS-induced cardiac injury through alleviation of ferroptosis.","authors":"Mai Chen, Pengchao Ma, Jingxing Liang, Shunming Zhu, Juan Ren","doi":"10.1080/08923973.2025.2507126","DOIUrl":"https://doi.org/10.1080/08923973.2025.2507126","url":null,"abstract":"<p><strong>Background: </strong>Ferroptosis-associated insults play a critical role in the pathological development of septic cardiomyopathy. Fenofibrate (Feno) is a fibrate drug used to treat high triglycerides and high cholesterol, however its pharmacological function in septic cardiomyopathy is not well understood.</p><p><strong>Materials and methods: </strong>We allocated 36 male C57BL/6J mice into four groups (<i>n</i> = 9/group): Vehicle, Feno, LPS, and LPS+Feno. Techniques included hematoxylin-eosin (HE) staining, LDH assay, ELISA, echocardiography, measurement of MDA, GSH, Fe2<sup>+</sup>, real-time PCR, and western blot analysis.</p><p><strong>Results: </strong>Administration of Feno significantly mitigated myocardial injury by reducing serum CK-MB levels from 963.8 U/L to 512.5 U/L, cTnI from 0.65 g/L to 0.36 g/L, and LDH from 552.4 U/L to 372.1 U/L. Feno improved cardiac function by increasing ejection fraction from 65.5% to 78.5% and fractional shortening from 42.3% to 57.3%. Feno also inhibited inflammatory cytokines IL-6 and TNF-α, reduced MDA levels, increased GSH levels, and restored GPX4, FTH1, and SLC7A11 expression. The protective effects of Feno may be associated with the YAP1 signaling pathway.</p><p><strong>Conclusion: </strong>Our findings suggest that Feno has the potential to protect against LPS-induced cardiac injury through the alleviation of ferroptosis, offering a promising therapeutic strategy for septic cardiomyopathy. However, the study is limited by the use of a single animal model and the lack of translational data in humans.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-9"},"PeriodicalIF":2.9,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sevoflurane induces cognitive dysfunction by modulating PER2 methylation to block AKT pathway-suppressed NLRP3 inflammatory vesicle in microglia.","authors":"Shuangjiang Li, Bin Wang","doi":"10.1080/08923973.2025.2496666","DOIUrl":"https://doi.org/10.1080/08923973.2025.2496666","url":null,"abstract":"<p><strong>Background: </strong>The anesthetic sevoflurane can cause cognitive dysfunction and may be involved in mediating DeoxyriboNucleic Acid (DNA) methylation. In this study, we dig into the mechanism of sevoflurane inducing cognitive dysfunction <i>via</i> DNA methylation pathway.</p><p><strong>Methods: </strong><i>In vivo</i> and <i>in vitro</i> experiments were performed in sevoflurane-induced rat models and microglia. <i>In vivo</i> experiments included Morris water maze, Western blot, methylation analysis and immunofluorescence, while <i>in vitro</i> experiments consisted of quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. MK2206 was used as a protein kinase B (AKT) inhibitor.</p><p><strong>Results: </strong>Sevoflurane induced cognitive dysfunction in rats, promoted levels of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), Interleukin (IL)-18, IL-1β, and ionized calcium-binding adapter molecule 1 (Iba-1) proteins, and inhibited Period2 (PER2) expression by enhancing methylation modification. PER2 was found to be located in microglia. Sevoflurane activated DNA methyltransferases (DNMTs) expression and suppressed PER2 <i>in vitro</i>. PER2 overexpression reduced NLRP3 inflammasomes-related protein expressions and restored AKT activation in sevoflurane-treated cells. Furthermore, MK2206 reversed the inhibitory effect of PER2 overexpression on cellular inflammation and AKT pathway activation.</p><p><strong>Conclusion: </strong>Sevoflurane affects AKT pathway-suppressed NLRP3 inflammasomes in microglia by modulating PER2 methylation, thereby contributing to cognitive dysfunction.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-9"},"PeriodicalIF":2.9,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144182110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Therapeutic efficacy of tofacitinib in PDSAg-induced chronic experimental autoimmune uveitis in Wistar rat.","authors":"Berru Yargi-Ozkocak, Ozlem Tugce Cilingir-Kaya, İrem Peker Eyuboglu, Can Erzik, Haner Direskeneli, Hande Celiker","doi":"10.1080/08923973.2025.2508278","DOIUrl":"https://doi.org/10.1080/08923973.2025.2508278","url":null,"abstract":"<p><strong>Purpose: </strong>Tofacitinib, a small molecule pan-JAK inhibitor, targets key inflammatory pathways that play a pivotal role in the pathophysiology of uveitis. Its ability to inhibit multiple cytokine signaling pathways makes it a promising candidate for the treatment of ocular inflammation. This study aimed to investigate the effect of oral tofacitinib on peptide-derived S-antigen (PDSAg)-induced chronic experimental autoimmune uveitis (EAU) in rats.</p><p><strong>Materials and methods: </strong>Nineteen albino Wistar rats were divided into five groups. Groups 1-3 (5 rats each) were immunized with 15 micrograms PDSAg to induce EAU; Group 2 received tofacitinib (5 mg/kg) by gavage twice daily. Group 3 received saline in the same manner as Group 2. Group 4 (2 rats) was a healthy control group. Group 5 (2 rats) received only tofacitinib. Uveitis development and treatment efficacy were evaluated using clinical scoring based on the the signs of anterior segment inflammation and histological scoring based on the deterioration of the retinal architectural structure.</p><p><strong>Results: </strong>Uveitis confirmed based on histological evidence was observed in all EAU groups (Groups 1-3) compared to the healthy control group (Group 4) (<i>p</i> < 0.001, <i>Mann-Whitney U test</i>). Tofacitinib significantly delayed the onset of uveitis in Group 2 when compared with Groups 1 and 3, which did not receive tofacitinib (<i>p</i> < 0.001, <i>Mann-Whitney U test</i>). Histological scores also showed a trend toward reduction (<i>p</i> = 0.393, <i>Mann-Whitney U test</i>).</p><p><strong>Conclusions: </strong>Oral tofacitinib delayed uveitis onset and reduced clinical and histological findings, suggesting its potential as an alternative treatment for uveitis.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-9"},"PeriodicalIF":2.9,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144158419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marc Henry, Takunda Ngwegya, Nkhasi Lekena, Stefan Barth
{"title":"<i>In vitro</i> anti-tumor activities of a novel recombinant immunotoxin targeting differentially overexpressed Leucine-rich repeat-containing G-protein-coupled receptor 5 in cervical cancer.","authors":"Marc Henry, Takunda Ngwegya, Nkhasi Lekena, Stefan Barth","doi":"10.1080/08923973.2025.2504904","DOIUrl":"10.1080/08923973.2025.2504904","url":null,"abstract":"<p><strong>Objective: </strong>The study aims to develop a novel recombinant anti-LGR5 immunotoxin candidate based on a truncated form of <i>Pseudomonas</i> exotoxin A (ETA).</p><p><strong>Methods: </strong>To develop this LGR5-specific recombinant immunotoxin, a corresponding single chain antibody fragment (αLGR5(scFv)) fused to ETA, was expressed under osmotic stress in the presence of compatible solutes in <i>Escherichia coli</i> BL21 DE3 cells. Expression was monitored by Western blot analysis facilitated by an N-terminal 10x-His tag. Purification was done using immobilized metal affinity chromatography (IMAC) and size exclusion chromatography (SEC). The recombinant immunotoxin (rIT) was assessed for cell surface binding on cervical cancer cell lines using confocal microscopy and flow cytometry. The rIT was then used in an XTT cell viability assay to assess targeted cell killing.</p><p><strong>Results and discussion: </strong>Upon confirmation of full-length protein by Western blot, purified protein was used to confirm binding on LGR5-positive cervical cancer cell lines <i>via</i> confocal microscopy and flow cytometry using anti-His PE antibody as a secondary antibody. Selective cell-killing of this novel recombinant immunotoxin was illustrated by the dose-dependent reduction in cell viability at IC50 values in nanomolar concentrations on antigen-positive but not antigen-negative cell lines.</p><p><strong>Conclusions: </strong>In conclusion, the rIT described is a promising candidate to treat cervical cancer, which however, would finally need to be confirmed by preclinical <i>in vivo</i> studies.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-10"},"PeriodicalIF":2.9,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Alpha-cyperone ameliorates renal fibrosis and inflammation in mice with chronic kidney disease <i>via</i> NF-κB and Akt/Nrf2/HO-1 pathways.","authors":"Wei Chen, Jiansong Mao, Chun Li, Jinlian Ke","doi":"10.1080/08923973.2025.2507129","DOIUrl":"https://doi.org/10.1080/08923973.2025.2507129","url":null,"abstract":"<p><strong>Background: </strong>Renal fibrosis is a hallmark feature of chronic kidney disease (CKD) and contributes to local inflammation and impaired renal function. The study aimed to investigate the effects of an active compound, alpha-cyperone, on renal fibrosis, inflammation, and oxidative stress in CKD mice.</p><p><strong>Methods: </strong>After subtotal nephrectomy, mice were administered with alpha-cyperone (5, 10, and 20 mg/kg) or captopril (the positive control) daily <i>via</i> oral gavage. Masson trichrome staining and periodic Acid-Schiff staining were performed to measure fibrotic areas and renal histopathological changes. An enzyme-linked immunosorbent assay was conducted to measure inflammatory cytokine levels in mouse serum samples. Superoxide anion concentrations, reactive oxygen species (ROS) level, and superoxide dismutase (SOD) activity were analyzed. Immunohistochemistry was performed to detect inflammatory and oxidative stress markers (Ly6G and 8-OHdG) in mouse renal tissues. Protein levels of factors involved in NF-κB signaling and Akt/Nrf2/HO-1 signaling were quantified by western blotting.</p><p><strong>Results: </strong>Alpha-cyperone at the dose of 10 mg/kg significantly improved renal functions in CKD model mice and alleviated tubulointerstitial fibrosis, with effects comparable to those of captopril. After CKD modeling, serum levels of inflammatory mediators, Ly6G levels, superoxide anion activity, ROS levels, and 8-OHdG levels were markedly increased, while the activity of antioxidant enzyme SOD was reduced. All these changes were ameliorated by alpha-cyperone or captopril treatment. Moreover, alpha-cyperone inhibited the NF-κB signaling and activated the Akt/Nrf2/HO-1 signaling in renal tissues of CKD mice.</p><p><strong>Conclusion: </strong>Alpha-cyperone ameliorates renal fibrosis in CKD mice by inhibiting inflammation and oxidative stress <i>via</i> NF-κB and Akt/Nrf2/HO-1 pathways.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-11"},"PeriodicalIF":2.9,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Unexplained lymphadenopathy following adjuvant immunotherapy in a non-small cell lung cancer patient: a literature review and a rare case report.","authors":"Lila Liu, Ying Wei, Qijiu Chen, Hanlin Liang","doi":"10.1080/08923973.2025.2507130","DOIUrl":"https://doi.org/10.1080/08923973.2025.2507130","url":null,"abstract":"<p><strong>Background: </strong>Immune checkpoint inhibitors (ICIs) have shown significant advantages in the treatment of lung cancer. Several studies have reported immune-related adverse events (irAEs) induced by ICIs. However, in clinical practice, irAEs occasionally cause lymphadenopathy, which can be mistaken for tumor progression, making it more challenging to accurately assess the patient's condition.</p><p><strong>Case presentation: </strong>This research report documents a rare clinical case of a patient with early-stage non-small cell lung cancer (NSCLC) who developed systemic lymphadenopathy during treatment with a PD-1 ICI following surgical resection. The patient developed widespread lymphadenopathy during postoperative PD-1 antibody maintenance therapy, accompanied by a series of irAEs, including persistent low cortisol levels, sluggish responses, memory loss, and stiffness in distal limbs and shoulder joints. Given the clinical presentation, the possibility of lymph node metastasis from lung cancer could not be entirely excluded. However, lymph node biopsy revealed reactive hyperplasia. After receiving corticosteroid treatment, the enlarged lymph nodes significantly reduced in size, and the associated low cortisol symptoms disappeared. During subsequent follow-up, the patient showed significant improvement and maintained a relatively stable condition.</p><p><strong>Results: </strong>In cases of postoperative generalized lymphadenopathy in NSCLC patients, if tumor recurrence is suspected, careful consideration is needed, especially in the era of ICI therapy. Postoperative PD-1 antibody maintenance therapy may induce reactive lymphadenopathy, including mediastinal lymph nodes. It is hypothesized that PD-1 antibodies cause T-cell activation in the lymph nodes.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-5"},"PeriodicalIF":2.9,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Zerumbone modulates the expression of inflammatory mediators and antioxidant enzymes in TNF-α-stimulated human periodontal ligament cells.","authors":"Risa Okamoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Keiichi Hosaka","doi":"10.1080/08923973.2024.2445724","DOIUrl":"10.1080/08923973.2024.2445724","url":null,"abstract":"<p><strong>Objectives: </strong>Periodontal disease is a chronic inflammatory disease caused by periodontopathogenic bacteria, and its progression leads to periodontal tissue destruction and tooth loss. Zerumbone is a bioactive substance found in ginger (<i>Zingiber zerumbet</i>) and is known to have bioactive effects such as anticancer effects, but there have been no attempts to use it for periodontitis treatment. In addition, there have been no reports examining its effects on periodontal tissue component cells. In this experiment, we aimed to determine whether zerumbone affects the production of inflammatory mediators induced by tumor necrosis factor (TNF)-α in human periodontal ligament cells (HPDLCs), including its effects on signaling pathways.</p><p><strong>Methods: </strong>HPDLCs were stimulated by TNF-α (10 ng/ml) with or without zerumbone (6.25, 12.5, or 25 µM). Cytokine production in supernatant was determined using ELISA. Activation of signal transduction pathways and intracellular protein expression were investigated using the western blot analysis.</p><p><strong>Results: </strong>Zerumbone significantly suppressed TNF-α-induced production of CC chemokine ligand 2 (CCL2), CCL20, CXC chemokine ligand 10 (CXCL10), and interleukin-6 (IL-6) in HPDLCs. In addition, zerumbone decreased intercellular adhesion molecule-1 (ICAM-1) and cyclooxygenase-2 (COX-2) expression in TNF-α-stimulated HPDLCs. Furthermore, zerumbone suppressed activation of nuclear factor (NF)-κB and signal transducer and activator of transcription 3 (STAT3) pathways in TNF-α-treated HPDLCs. Finally, zerumbone enhanced the production of heme oxygenase-1 (HO-1), an antioxidant enzyme, in HPDLCs.</p><p><strong>Conclusion: </strong>These results suggest that zerumbone suppressed the production of several inflammatory mediators by inhibiting the NF-κB and STAT3 pathways in HPDLCs.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"176-181"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Semra Fırat, Şükran Erten, Serdar Can Güven, Sezen Tutar, Yüksel Maraş, Salim Neşelioğlu, Selçuk Akan, Ahmet Kor, Berkan Armağan, Kevser Orhan, İsmail Doğan, Orhan Küçükşahin, Özcan Erel
{"title":"Effect of biological treatment on the thiol/disulfide parameters in patients with axial spondyloarthritis.","authors":"Semra Fırat, Şükran Erten, Serdar Can Güven, Sezen Tutar, Yüksel Maraş, Salim Neşelioğlu, Selçuk Akan, Ahmet Kor, Berkan Armağan, Kevser Orhan, İsmail Doğan, Orhan Küçükşahin, Özcan Erel","doi":"10.1080/08923973.2025.2469211","DOIUrl":"10.1080/08923973.2025.2469211","url":null,"abstract":"<p><strong>Objective: </strong>Aim of this study is to compare the thiol/disulfide variables before treatment, at the 3<sup>rd</sup> and 6<sup>th</sup> months of biologic treatment in patients with axSpA.</p><p><strong>Materials & methods: </strong>Consecutive patients with axial spondyloarthritis to whom biologic treatment was initiated in our clinic were enrolled upon consent. Demographics, clinical characteristics, laboratory parameters and treatment agents were collected. Disease activity scores and thiol-disulfide balance parameters were recorded at baseline and 3<sup>rd</sup>, 6<sup>th</sup> months of treatment. Statistical analyses were performed in all patients and in subgroups of ankylosing spondylitis and non-radiographic axial spondyloarthritis patients.</p><p><strong>Results: </strong>In all patients, total thiol levels were significantly increased at 6<sup>th</sup> month in comparison to baseline values (470.5 ± 74.7 vs 491.9 ± 69.6, <i>p</i> = 0.047). Native thiol levels were increased at 6<sup>th</sup> month close to significance (438.9 ± 70.4 vs 458.8 ± 63.7, <i>p</i> = 0.060). Moderately strong negative correlations were observed between native thiol levels and disease activity parameters (BASDAI: <i>p</i> = 0,019; ASDAS-CRP: <i>p</i> = 0,035; ASDAS-ESR: <i>p</i> = 0,030), and between total thiol levels and disease activity parameters (BASDAI: <i>p</i> = 0,031; ASDAS-CRP: <i>p</i> = 0,020; ASDAS-ESR: <i>p</i> = 0,026) at 6<sup>th</sup> month evaluation.</p><p><strong>Discussion & conclusions: </strong>Our results demonstrated oxidative stress reducing effect of biologics in axSpA patients parallel to suppression of disease activity at 6<sup>th</sup> month of the treatment.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"228-233"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}