Immunopharmacology and Immunotoxicology最新文献

{"title":"Evaluating the impact of amitriptyline on Nitric Oxide signaling in rat models of neuropathic pain.","authors":"Hamid Reza Mohammadi, Zahra Haghighatian, Behrouz Beiranvand, Peyman Amanolahi Baharvand, Amin Hasanvand","doi":"10.1080/08923973.2025.2481870","DOIUrl":"https://doi.org/10.1080/08923973.2025.2481870","url":null,"abstract":"<p><strong>Introduction: </strong>Nitric oxide (NO) plays a crucial role in the induction of neuropathic pain by stimulating the production of inflammatory cytokines. Additionally, research indicates that amitriptyline can inhibit nitric oxide production. In this study, we examined the inhibitory role of the nitric oxide signaling pathway through the administration of amitriptyline in the treatment of neuropathic pain.</p><p><strong>Methods: </strong>Forty rats were randomly assigned to five groups, with eight animals in each group: (1) Sham-operated, (2) Chronic constriction injury (CCI), (3) CCI plus amitriptyline, (4) CCI plus amitriptyline and L-arginine, and (5) CCI plus amitriptyline and L-NAME. Behavioral tests, including thermal hyperalgesia, cold allodynia, and mechanical allodynia, were conducted on the fourth, seventh, and fourteenth days following CCI induction. On the final day, spinal cord samples were collected to assess the levels of inflammatory cytokines. Additionally, the sciatic nerve was isolated on the same day for histological examination.</p><p><strong>Results: </strong>The results indicated that the administration of amitriptyline can reduce levels of inflammatory cytokines and improve symptoms of neuropathic pain. It should be noted that the simultaneous use of L-NAME and amitriptyline increases the therapeutic impacts of amitriptyline. However, the beneficial effects of amitriptyline are reduced by the nitric oxide stimulation induced by L-arginine.</p><p><strong>Conclusion: </strong>It was determined that one of the mechanisms by which amitriptyline ameliorates neuropathic pain is the inhibition of the nitric oxide signaling pathway. In this study, this effect was associated with a reduction in the release of inflammatory cytokines and a decrease in inflammation surrounding the nerve.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-9"},"PeriodicalIF":2.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772239","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}

{"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^rd and 6^th 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^rd, 6^th 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^th 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^th 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^th 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^th 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}

{"title":"Efficacy and safety of ibuprofen and naproxen in the treatment of oligoarticular juvenile idiopathic arthritis: bi-national cohort study.","authors":"Orly Ohana, Itay Marmor, Rina Ferguson, Yoel Levinsky, Shiri Rubin, Kevin Baszis, Rotem Tal, Liora Harel, Orit Peled, Gil Amarilyo","doi":"10.1080/08923973.2024.2421523","DOIUrl":"10.1080/08923973.2024.2421523","url":null,"abstract":"<p><strong>Objectives: </strong>Juvenile idiopathic arthritis (JIA) is the most common rheumatic disease in children. Nonsteroidal anti-inflammatory drugs (NSAIDs) and intra-articular corticosteroid injections are first-line therapy for oligoarticular JIA. NSAIDs Adverse events (AEs) include gastrointestinal ulcers/bleeding and impaired renal function. The most prescribed NSAIDs for oligoarticular JIA are ibuprofen and naproxen. However, direct comparison between these drugs is lacking. We aimed to compare the efficacy and safety of ibuprofen versus naproxen for oligoarticular JIA.</p><p><strong>Methods: </strong>This is a bi-national retrospective study of oligoarticular JIA patients treated with either ibuprofen or naproxen as first-line therapy. Efficacy was defined as patients that achieved complete response (no evidence for arthritis). Safety was assessed by the occurrence of adverse events during follow-up.</p><p><strong>Results: </strong>Of 164 patients, 103 were treated in the Israeli group and 61 in the US group. The study population had a mean age of 4.49 ± 3.55 years, with F:M ratio of ∼2.5:1. No significant difference was found in drug efficacy [Complete response was observed in 15% of the ibuprofen group <i>vs</i>. 17.3% in naproxen group (<i>p</i> = 0.7)]. Treatment duration > 28 days was associated with significantly higher odds for complete response (<i>p</i> = 0.021). For safety, 12 AEs were associated with naproxen, whereas no AEs were associated with ibuprofen (<i>p</i> = 0.004). Treatment was discontinued in all AEs cases.</p><p><strong>Conclusions: </strong>Ibuprofen and naproxen showed similar albeit low efficacy which emphasizes their role as bridging therapy until IACI is achieved. However, ibuprofen showed better safety profile naproxen and therefore should be considered as first-line therapy.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"141-146"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142948211","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":"Evaluation of the inhibitory effect of different molecular weights chitosan on MRGPRX2-mediated mast cell degranulation and the pseudo-allergic reaction.","authors":"Dewu Zhang, Ruiqi Li, Liping Liu, Ruijuan Lu, Juan Li, Yajing Hou","doi":"10.1080/08923973.2025.2457971","DOIUrl":"10.1080/08923973.2025.2457971","url":null,"abstract":"<p><strong>Objectives: </strong>Chitosan is widely used in medicine to regulate immune responses in T cells and dendritic cells. However, research on the regulation of mast cells (MCs) is scarce. Mas-related G-protein-coupled receptor X2 (MRGPRX2) is a key receptor that mediates MC activation. However, the inhibitory effects of chitosan on MRGPRX2 activation have not yet been reported. The aim of this study was to determine whether chitosan inhibits MRGPRX2-mediated MC activation and the molecular weight of chitosan with the best inhibitory effect.</p><p><strong>Methods: </strong>Cytotoxic and activating effects of chitosan on LAD2 cells were evaluated <i>in vitro</i>. An <i>in vitro</i> MC degranulation reaction model and <i>in vivo</i> C48/80-induced local passive anaphylaxis mouse model were used to evaluate the inhibitory effect of chitosan on MRGPRX2 activation.</p><p><strong>Key findings: </strong>Chitosan inhibited MC degranulation mediated by MRGPRX2 <i>in vitro</i> and reduced histamine, β-hexosaminidase, and cytokine release. Chitosan inhibited local pseudo-allergy and inflammatory mediator release by inhibiting MRGPRX2-mediated MC activation. Moreover, low-molecular-weight chitosan exhibited superior inhibitory activity against MRGPRX2.</p><p><strong>Conclusions: </strong>Chitosan inhibited MRGPRX2-mediated MC degranulation <i>in vivo</i> and <i>in vitro</i>. Low molecular weight chitosan has the potential to be developed as a functional drug or food to assist in the treatment of MRGPRX2-regulated diseases.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"213-221"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023293","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":"Ruxolitinib enhances gastric cancer to chemotherapy by suppressing JAK/STAT3 and inducing mitochondrial dysfunction and oxidative stress.","authors":"Yang Yao, Jun Zhou, Jing Song, Cheng Chen","doi":"10.1080/08923973.2025.2470344","DOIUrl":"10.1080/08923973.2025.2470344","url":null,"abstract":"<p><strong>Objective: </strong>Chemoresistance in gastric cancer poses a major challenge in treatment, necessitating the development of novel therapeutic strategies. This study evaluates the efficacy of ruxolitinib, a JAK1/2 inhibitor, in both sensitive and resistant gastric cancer cell lines.</p><p><strong>Materials and methods: </strong>Gastric cancer cell lines, including sensitive (N87 and AGS) and resistant (N87-R and AGS-R) variants, were treated with ruxolitinib alone or in combination with chemotherapeutic agents. Apoptosis induction, mitochondrial function, oxidative stress, and key signaling pathways were analyzed. Tumor growth, p-STAT3 levels, and overall survival were evaluated in xenograft models.</p><p><strong>Results: </strong>Ruxolitinib induced dose-dependent mitochondrial-mediated apoptosis in resistant cells and enhanced cytotoxicity in combination with chemotherapy in sensitive cells. The treatment inhibited phosphorylation of STAT3, Akt, and mTOR. Additionally, ruxolitinib reduced basal and maximal respiration rates while increasing ROS levels, suggesting mitochondrial dysfunction and oxidative stress. Resistant cells exhibited increased mitochondrial DNA content, elevated respiration rates, and higher ROS levels compared to sensitive cells, indicating alterations in mitochondrial biogenesis and redox homeostasis. These findings were supported by changes in gene expression related to mitochondrial function. In vivo, ruxolitinib significantly inhibited tumor growth and reduced p-STAT3 levels in resistant gastric cancer xenografts without causing significant weight loss. Furthermore, ruxolitinib treatment significantly prolonged overall survival in mice.</p><p><strong>Conclusion: </strong>Ruxolitinib demonstrates potential in overcoming chemoresistance in gastric cancer by targeting mitochondrial function, oxidative stress, and key survival pathways. These findings support further investigation into its clinical application as an adjunct therapy for chemoresistant gastric cancer.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"263-271"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515375","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":"Albiflorin ameliorates neuroinflammation and exerts neuroprotective effects in Parkinson's disease models.","authors":"Yuan Gao, Yanmei Chen, Ning Wang, Qiang Meng","doi":"10.1080/08923973.2025.2457960","DOIUrl":"10.1080/08923973.2025.2457960","url":null,"abstract":"<p><strong>Background: </strong>Albiflorin isolated from <i>Paeoniae Alba Radix</i> can cross the blood-brain barrier (BBB) and possesses analgesia, anticonvulsant, anti-inflammatory, and hepatoprotective properties. This study investigates albiflorin functions and related mechanisms in Parkinson's disease (PD) pathogenesis.</p><p><strong>Methods: </strong>Cellular and animal models of PD were constructed. Cell viability and apoptosis were detected by CCK-8 assays. Levels of Iba-1 and TH were measured by immunofluorescence staining, western blotting, and immunohistochemistry staining. Levels of pro-inflammatory mediators and pathway-related genes were measured by western blotting and RT-qPCR. Locomotor activity of mice was examined by open field test, rod climbing test, and rod rotating test.</p><p><strong>Results: </strong>For <i>in vitro</i> analysis, albiflorin inhibited LPS-induced microglial activation and neuroinflammation. Additionally, albiflorin inactivated NF-κB and MAPK pathways in LPS-treated BV2 cells. Moreover, albiflorin attenuated neurotoxicity mediated by LPS-stimulated microglia. For <i>in vivo</i> analysis, albiflorin improved MPTP-induced locomotor activity deficits and reduced MPTP-induced dopaminergic neuron loss. In parallel, albiflorin inhibited activated microglia-mediated neuroinflammation in MPTP-treated mice.</p><p><strong>Conclusion: </strong>Albiflorin mitigates neuronal apoptosis and improves behavioral impairments in MPTP-induced PD mouse model through inhibition of activated microglia-mediated neuroinflammation <i>via</i> the NF-κB and MAPK pathways.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"201-212"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382382","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":"Combination therapies and other therapeutic approaches targeting the NLRP3 inflammasome and neuroinflammatory pathways: a promising approach for traumatic brain injury.","authors":"Zana Montazeri-Khosh, Ahmad Ebrahimpour, Mina Keshavarz, MohammadHosein Sheybani-Arani, Afshin Samiei","doi":"10.1080/08923973.2024.2444956","DOIUrl":"https://doi.org/10.1080/08923973.2024.2444956","url":null,"abstract":"<p><strong>Objectives: </strong>Traumatic brain injury (TBI) precipitates a neuroinflammatory cascade, with the NLRP3 inflammasome emerging as a critical mediator. This review scrutinizes the complex activation pathways of the NLRP3 inflammasome by underscoring the intricate interplay between calcium signaling, mitochondrial disturbances, redox imbalances, lysosomal integrity, and autophagy. It is hypothesized that a combination therapy approach-integrating NF-κB pathway inhibitors with NLRP3 inflammasome antagonists-holds the potential to synergistically dampen the inflammatory storm associated with TBI.</p><p><strong>Methods: </strong>A comprehensive analysis of literature detailing NLRP3 inflammasome activation pathways and therapeutic interventions was conducted. Empirical evidence supporting the concurrent administration of MCC950 and Rapamycin was reviewed to assess the efficacy of dual-action strategies compared to single-agent treatments.</p><p><strong>Results: </strong>Findings highlight potassium efflux and calcium signaling as novel targets for intervention, with cathepsin B inhibitors showing promise in mitigating neuroinflammation. Dual therapies, particularly MCC950 and Rapamycin, demonstrate enhanced efficacy in reducing neuroinflammation. Autophagy promotion, alongside NLRP3 inhibition, emerges as a complementary therapeutic avenue to reverse neuroinflammatory damage.</p><p><strong>Conclusion: </strong>Combination therapies targeting the NLRP3 inflammasome and related pathways offer significant potential to enhance recovery in TBI patients. This review presents compelling evidence for the development of such strategies, marking a new frontier in neuroinflammatory research and therapeutic innovation.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":"47 2","pages":"159-175"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730082","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":"C-phycocyanin acts as a positive immunomodulator in different primary and secondary organs of mice.","authors":"Mariana Teixeira Santos Figueiredo Salgado, Mayara Cristini Sebastião Silva, Ricardo Correia da Silva, Maria Luísa Arantes Campos, Camilly Fratelli, Anna Rafaela Cavalcante Braga, Milena Barcza Stockler-Pinto, Ana Paula de Souza Votto, Luciana Souza de Paiva","doi":"10.1080/08923973.2024.2448801","DOIUrl":"10.1080/08923973.2024.2448801","url":null,"abstract":"<p><strong>Objective: </strong>C-Phycocyanin (C-PC) is a photosynthetic pigment with interesting therapeutic properties. However, its effectiveness in modulating the immune system cell populations has not been elucidated. We analyzed the action of C-PC on the modulation of mice immune system.</p><p><strong>Methods: </strong>The animals were treated subcutaneously with C-PC for 3 consecutive days. On the fourth day, the animals were euthanized and cells from different organs were analyzed by flow cytometry. Cytotoxicity was analyzed using biochemical parameters.</p><p><strong>Results: </strong>The results showed that C-PC increased the total cellularity in percentage and absolute number in the inguinal lymph node as well as the absolute number of B cells, CD4+ and CD8+ T cells and myeloid cells. The percentage of B cells was also increased in the lymph node. In the bone marrow, there was a reduction in immature and mature B cells. In contrast, C-PC increased the percentage and absolute number of myeloid cells in the bone marrow. C-PC administration also promoted an increase of CD4+ and CD8+ T cells in the thymus, and a reduction in these populations in the spleen.</p><p><strong>Conclusion: </strong>The data show for the first time the positive immunomodulatory role of C-PC by recruiting distinct populations of immune system cells to the treatment-draining lymphoid organ.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"182-193"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004580","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":"Potential regulation of artesunate on bone metabolism through suppressing inflammatory infiltration in type 2 diabetes mellitus.","authors":"Jinghong Luo, Kun Chen, Xiaolin Nong","doi":"10.1080/08923973.2024.2444953","DOIUrl":"https://doi.org/10.1080/08923973.2024.2444953","url":null,"abstract":"<p><strong>Objective: </strong>Osteoimmunology is an emerging field that explores the interplay between bone and the immune system. The immune system plays a critical role in the pathogenesis of diabetes and significantly affects bone homeostasis. Artesunate, a first-line treatment for malaria, is known for its low toxicity and multifunctional properties. Increasing evidence suggests that artesunate possesses anti-inflammatory, immunoregulatory, and osteogenic effects. This review aims to explore the relationship between immune regulation and bone metabolism in type 2 diabetes (T2DM) and to investigate the potential therapeutic application of artesunate.</p><p><strong>Methods: </strong>This review systematically examines literature from PubMed/Medline, Elsevier, Web of Science, Embase, the International Diabetes Federation, and other relevant databases.</p><p><strong>Results: </strong>This review synthesizes evidence from multiple sources to delineate the relationship between T lymphocytes and T2DM, the regulation of T lymphocyte subsets in bone metabolism, and the effects of artesunate on both T lymphocytes and bone metabolism. Recent studies suggest a bidirectional regulatory relationship between T2DM and T lymphocytes (CD4⁺ T and CD8⁺ T) during the onset and progression of the disease, with inflammatory and anti-inflammatory cytokines serving as key mediators. T lymphocyte subsets and their cytokines play a pivotal role in regulating osteogenesis and osteoclastogenesis in pathological conditions. Furthermore, artesunate has shown promise in modulating inflammatory infiltration and bone metabolism.</p><p><strong>Conclusion: </strong>The accumulated evidence indicates that artesunate exerts regulatory effects on bone metabolism in T2DM by influencing T lymphocyte differentiation.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":"47 2","pages":"147-158"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730083","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}