Immunopharmacology and Immunotoxicology最新文献

{"title":"Protective effect of nebivolol on bleomycin-induced lung fibrosis via suppressing TLR4/IL-1β/MMP-2 and TGF-β/HSP47 signaling pathways in rats.","authors":"Mohamed A Morsy, Seham A Abdel-Gaber, Mohamed F Abed El Baky, Sara Mohamed Naguib Abdel Hafez, Anroop B Nair, Katharigatta N Venugopala, Pottathil Shinu, Yasmine F Ibrahim","doi":"10.1080/08923973.2026.2655392","DOIUrl":"10.1080/08923973.2026.2655392","url":null,"abstract":"<p><strong>Background: </strong>Idiopathic pulmonary fibrosis (IPF), a potentially fatal illness, significantly alters normal lung structure and function, resulting in severe respiratory failure and death. As of yet, no curable remedy has been revealed. Nebivolol is a third-generation β-blocker that has numerous cytoprotective properties and is used to treat heart failure and hypertension. Its potential ability to prevent bleomycin-induced IPF has not been studied. The aim of the current study is to investigate the antifibrotic effect of nebivolol against bleomycin-induced lung fibrosis.</p><p><strong>Methods: </strong>Twenty-four male Wistar rats were randomly divided into four groups (<i>n</i> = 6 per group): control, bleomycin, nebivolol, and nebivolol + bleomycin. Pulmonary fibrosis was induced by bleomycin administration, while nebivolol was given seven days prior to a single intratracheal injection of bleomycin, daily orally for 21 days. At the end of the study, lung injury and fibrosis were evaluated using histopathological analysis, lung wet/dry ratio, bronchoalveolar lavage fluid protein content, oxidative stress markers, inflammatory cytokines, and fibrosis-related signaling.</p><p><strong>Results: </strong>Nebivolol significantly decreased the histopathological injuries demonstrated through lung tissue sections stained by hematoxylin/eosin and silver. It considerably decreased the lung wet/dry ratio, as well as the total protein level in bronchoalveolar lavage fluid. Further, nebivolol restored superoxide dismutase activity and suppressed elevated malondialdehyde levels, rebalancing the disrupted oxidative indicators. Nebivolol is additionally known to have anti-inflammatory effects, as demonstrated by a decrease in cytokine levels, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), while boosting the secretion of the anti-inflammatory mediator endothelial nitric oxide synthase. In addition, nebivolol's anti-inflammatory properties were obvious by its suppressing effect on Toll-like receptor 4 (TLR4) level and the matrix metalloproteinase-2 (MMP-2) expression. Finally, nebivolol mitigated the progression of the fibrotic cascade, as indicated by reducing the elevated levels of transforming growth factor beta (TGF-β) and heat shock protein 47 (HSP47).</p><p><strong>Conclusion: </strong>Nebivolol treatment exhibited remarkable protective effects on bleomycin-mediated IPF in rats <i>via</i> suppressing TLR4/IL-1β/MMP-2 and TGF-β/HSP47 signaling pathways. This study might provide an innovative therapeutic approach to prevent the devastating lung scarring associated with IPF.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"375-387"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644913","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":"Promising efficacy of coenzyme Q10 supplementation as adjunctive therapy in juvenile idiopathic arthritis: a randomized-controlled pilot study.","authors":"Nourhan Elsherif, Ghada Shousha, Nagwa Ali Sabri, May Ahmed Shawki","doi":"10.1080/08923973.2026.2657954","DOIUrl":"10.1080/08923973.2026.2657954","url":null,"abstract":"<p><strong>Background: </strong>Coenzyme Q10 (CoQ10), a potent antioxidant and anti-inflammatory agent, has shown therapeutic promise in adult autoimmune disorders. However, its role in juvenile idiopathic arthritis (JIA) has not been explored.</p><p><strong>Objective: </strong>To evaluate the efficacy and safety of oral CoQ10 in JIA patients.</p><p><strong>Materials and methods: </strong>In this prospective, single-blinded-pilot trial, 58 patients with active JIA were randomized equally to receive either CoQ10 (100 mg/day) or placebo plus standard therapy for 3 months. Clinical outcome was assessed using Juvenile Arthritis Disease Activity Score (JADAS-10). The quality of life (QoL) was evaluated using Childhood Health Assessment Questionnaire (CHAQ). Biochemical markers included tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), and glutathione (GSH). All parameters were assessed at baseline and after 3 months.</p><p><strong>Results: </strong>Fifty-one patients completed the study. The median percent change of JADAS score in the CoQ10 group was -49.1 which was significantly lower than the control group with a median percent change of 2, <i>p</i> < 0.001. Within-group and between groups comparisons showed that the QoL significantly improved in the CoQ10 group compared to the control group (median percent change -60 vs. -33 respectively, <i>p</i> < 0.001). Same positive effects were observed on serum biomarkers whereas median percent changes in the CoQ10 group versus control group were -29.1 vs. -4.3, -44.4 vs. 2, and 12.1 vs. -5.1 for TNF-α, MDA and GSH respectively (all <i>p</i> < 0.01). Minor side-effects were reported during the study.</p><p><strong>Conclusion: </strong>CoQ10 significantly improved disease severity, QoL, and inflammatory and oxidative stress markers in JIA patients with an excellent safety profile.</p><p><p><b>Clinical-trials.gov identification number:</b> NCT05871086.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"388-395"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644900","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":"Vildagliptin alleviates cardiomyocyte apoptosis and inflammatory responses in the treatment of non-valvular atrial fibrillation by regulating the NO/sGC/cGMP signaling pathway.","authors":"Zhaodi Wang, Zhihan Zhao, Xiaobiao Zang, Lei Wang, Yonghui Zhao","doi":"10.1080/08923973.2026.2639559","DOIUrl":"10.1080/08923973.2026.2639559","url":null,"abstract":"<p><strong>Aim: </strong>to investigate the therapeutic effects of vildagliptin on non-valvular atrial fibrillation (NVAF) and to determine whether its underlying mechanism of action is associated with modulation of the nitric oxide/soluble guanylate cyclase/cyclic guanosine monophosphate (NO/sGC/cGMP) signaling pathway.</p><p><strong>Methods: </strong>Thirty clean-grade male Sprague-Dawley (SD) rats were enrolled. Atrial fibrillation was first induced by electrical stimulation of the vagus nerve. After confirming postoperative survival in all animals, the rats were randomly assigned to a normal control group (CG), an atrial fibrillation group (AFG), and a drug-treated group (DG), thereby establishing an NVAF rat model. Myocardial electro-physiological parameters, levels of inflammatory cytokines, the cardiomyocyte apoptosis index (AI), as well as nitric oxide (NO), cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), and soluble guanylate cyclase (sGC) were measured and compared among the three groups.</p><p><strong>Results: </strong>Compared with the CG, the AFG exhibited significantly reduced effective refractory period (ERP), action potential duration at 90% repolarization (APD90), and the ERP/APD90 ratio, accompanied by markedly elevated levels of inflammatory cytokines and a higher AI. In addition, concentrations of NO, cAMP, and cGMP were significantly decreased, sGC expression was downregulated, and phosphodiesterase 5 A (PDE5A) expression was upregulated (all <i>p</i> < 0.05). In comparison with the AFG, rats in the DG showed significant increases in ERP, APD90, and the ERP/APD90 ratio, along with pronounced reductions in inflammatory cytokine levels and cardiomyocyte AI.</p><p><strong>Conclusion: </strong>Vildagliptin can markedly improve the myocardial electrical and vascular functions and reduce cardiomyocyte apoptosis and inflammatory responses in NVAF.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"404-413"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770365","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":"Nanomedicine carrier-based combined antitumor strategy integrating phototherapy and immunotherapy.","authors":"Yang Yan, Zhiyuan Gu, Dan Mao, Yuanna Zheng","doi":"10.1080/08923973.2026.2671715","DOIUrl":"10.1080/08923973.2026.2671715","url":null,"abstract":"<p><strong>Introduction: </strong>The combination of phototherapy (PTT/PDT) and immunotherapy holds promise for cancer treatment but is hindered by poor spatiotemporal coordination and inadequate targeted co-delivery. Nanomedicine carriers offer a platform to overcome these barriers by enabling precise control over drug release kinetics and reducing off-target toxicity. Methods This review systematically analyzes the rationale, mechanisms, and recent advances in nanocarrier-mediated phototherapy-immunotherapy combination strategies, with a focus on studies published within the last three years. We examine how nanocarriers enable targeted co-delivery, stimuli-responsive release, and enhanced tumor accumulation of phototherapeutic agents and immunomodulators.</p><p><strong>Results: </strong>Phototherapy induces immunogenic cell death (ICD) characterized by calreticulin exposure, ATP secretion, and high-mobility group box 1 (HMGB1) release, which primes dendritic cells and initiates adaptive immunity. Nanocarriers facilitate precise spatiotemporal orchestration of these signals and enable co-delivery with immune checkpoint inhibitors, in situ vaccines, immunomodulators, and adoptive cell therapies, including chimeric antigen receptor (CAR)-T cells. Key outcomes include conversion of \"cold\" to \"hot\" tumors, enhanced T-cell infiltration, abscopal effects, and durable immune memory in preclinical models. Emerging trends include multi-responsive nanoplatforms, biomimetic designs, and hypoxia-overcoming strategies that restore antitumor immunity.</p><p><strong>Discussion: </strong>Despite compelling preclinical success, challenges remain in clinical translation, including manufacturing scalability, human tumor heterogeneity, and optimal treatment sequencing. Future directions point towards personalized nanoplatforms, multimodal synergy, and the integration of artificial intelligence and synthetic biology. In conclusion, nanocarrier-mediated phototherapy-immunotherapy integration offers a powerful and evolving approach to achieve durable antitumor immunity and holds transformative potential for solid tumor treatment.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"479-494"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972100","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":"Investigation of the nitric oxide signaling pathway induced by ezetimibe on renal injury in streptozotocin-induced diabetic rat: role of anti-oxidative and anti-inflammatory effects.","authors":"Amin Hasanvand, Amin Rezaei Ghaleh, Bahram Delfan, Azita Zafar Mohtashami, Zahra Haghighatian, Elham Goodarzi, Babak Hadian","doi":"10.1080/08923973.2026.2657952","DOIUrl":"10.1080/08923973.2026.2657952","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetes is a disease characterized by impaired insulin secretion and/or function. Ezetimibe is a lipid-lowering drug widely used for the treatment of hypercholesterolemia. This study investigates the impact of ezetimibe on nitric oxide level and its effects on diabetic nephropathy.</p><p><strong>Materials & methods: </strong>Sixty rats were used in the study, divided into the following groups: a control group (healthy rats), a diabetic control group, a diabetic group treated with metformin, a diabetic group treated with ezetimibe, a diabetic group treated with ezetimibe plus L-NAME, and a diabetic group treated with ezetimibe plus L-arginine. After 28 days, blood samples were collected and rats were euthanized to examine nitric oxide levels and kidney histology. The levels of creatinine, urea, glutathione peroxidase (GPx), catalase (CAT), tumor necrosis factor (TNF-α), and interleukin (IL-6) were measured.</p><p><strong>Results: </strong>Ezetimibe treatment resulted in decreased levels of urea and creatinine in blood samples, along with reduced TNF-α and IL-6 levels in the kidneys. Additionally, GPx and CAT levels significantly increased following ezetimibe treatment. Our findings showed that the combination of ezetimibe and L-arginine provided protection against nephropathy in the animals, as demonstrated by enhanced antioxidant activity and reduced inflammation. However, the beneficial effects of ezetimibe were reversed by L-NAME.</p><p><strong>Conclusion: </strong>Ezetimibe protected the kidney against diabetic injury mainly by activating the nitric oxide signaling pathway, enhancing antioxidant enzyme activity, and reducing inflammation, suggesting that its nephroprotective effects are NO-dependent.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"428-436"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770437","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":"Medicarpin suppresses thyroid cancer progression by inhibiting the AKT/NF-κB pathway and enhancing CD8⁺ T cell-mediated antitumor immunity.","authors":"Zhitao Zhang, Xu Zhang, Yinping Yu, Xiaoming Zhang","doi":"10.1080/08923973.2026.2652318","DOIUrl":"10.1080/08923973.2026.2652318","url":null,"abstract":"<p><strong>Background: </strong>Poorly differentiated and anaplastic thyroid cancers exhibit resistance to treatment and immune evasion. Medicarpin (MED), a natural pterocarpan derived from leguminous plants, has shown anticancer activity in multiple tumor models. This study investigated the effects of MED on thyroid cancer progression.</p><p><strong>Methods: </strong>Thyroid cancer cell lines (8505 C, TPC-1) and normal thyroid epithelial cells (Nthy-ori 3-1) were treated with varying concentrations of MED. Proliferation, apoptosis, and protein expression were evaluated using CCK-8, Hoechst staining, flow cytometry, ELISA, Western blot, and immunofluorescence. Tumor-immune interactions were assessed <i>via</i> co-culture with CD8⁺ T cells. The AKT activator SC79 was used to verify the involvement of the pathway. <i>In vivo</i> effects were analyzed in humanized NOG mice bearing subcutaneous 8505 C xenografts.</p><p><strong>Results: </strong>No cytotoxicity was observed in Nthy-ori 3-1 cells treated with MED at concentrations ≤80 μM. but MED reduced cell viability in 8505 C and TPC-1 cells (IC₅₀: 62.20 μM for 8505 C, 70.84 μM for TPC-1). Apoptosis was confirmed by nuclear fragmentation and an increase in cleaved caspase-3. MED suppressed PD-L1 expression and CD8⁺ T cell apoptosis, while enhancing IFN-γ, TNF-α, and Granzyme B secretion. MED reduced phosphorylation and nuclear translocation of NF-κB <i>via</i> AKT inhibition, which SC79 partially reversed. <i>In vivo</i>, MED reduced tumor growth in humanized NOG mice, decreased PD-L1 and AKT/NF-κB signaling, enhanced CD8⁺ T-cell activation (CD69, IFN-γ), indicating immune-dependent antitumor activity.</p><p><strong>Conclusions: </strong>MED suppresses thyroid cancer progression by inhibiting proliferation and immune evasion through the inactivation of AKT/NF-κB, supporting its potential as a therapeutic candidate.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"363-374"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644956","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":"Aryl-Cyclohexanone as a potential CB2 agonist: <i>in vitro</i> and <i>in silico</i> evidence in inflammatory modulation.","authors":"Tainá Larissa Lubschinski, Luiz Antonio Escorteganha Pollo, Luigi Arruda Nardino, Roberto Gomes de Carvalho Filho, Ziliani da Silva Buss, Louis Pergaud Sandjo, Maique Weber Biavatti, Leonardo Bruno Federico, Eduardo Monguilhott Dalmarco","doi":"10.1080/08923973.2026.2655385","DOIUrl":"10.1080/08923973.2026.2655385","url":null,"abstract":"<p><strong>Background: </strong>Inflammation is an evolutionarily conserved adaptive process essential for host defense against harmful stimuli, aimed at restoring homeostasis. However, exacerbated or dysregulated responses are associated with the progression of several autoimmune and chronic inflammatory diseases, representing a significant clinical challenge. The endocannabinoid system has been described as an important immunomodulatory pathway in which synthetic cannabinoids exert immunosuppressive effects, providing novel therapeutic targets. Aryl-Cyclohexanone (AD) has previously demonstrated anti-inflammatory properties in both <i>in vitro</i> and <i>in vivo</i> models.</p><p><strong>Methods: </strong>Herein we aimed to investigate its immunomodulatory profile <i>in vitro</i>, using lipopolysaccharide (LPS)-induced inflammation in murine macrophages (J774), and its potential agonist action on CB2 receptor using human macrophages (THP-1), as well as confirm the specific and stable connection with cannabinoid receptor type 2 (CB2) through <i>in silico</i> docking and molecular dynamics analyses.</p><p><strong>Results: </strong>In J774 macrophages, AD treatment preserved cell viability, reduced nitric oxide metabolites production, normalized apoptotic events, and enhanced phagocytosis. Additionally, decreased Toll-like receptor 4 and increased mannose receptor (CD206) expressions were observed, along with a significant reduction in pro-inflammatory cytokines production (IL-12p70, TNF-α, IFN-γ, MCP-1, and IL-6). In THP-1 macrophages, the compound maintained its anti-inflammatory activity only in the absence of the selective CB2 inverse agonist (SR144528), preserving cell viability and reducing nitric oxide metabolites and pro-inflammatory cytokine production. These findings indicate that its immunomodulatory effect is directly associated with CB2 receptor interaction. Complementary <i>silico</i> analyses confirmed a specific and stable interaction with CB2 receptor, supporting a relevant agonistic activity observed in <i>in vitro</i> experiments.</p><p><strong>Conclusion: </strong>The results demonstrate that AD exerts significant anti-inflammatory and immunomodulatory effects, associated with CB2 receptor agonism, highlighting its potential as a promising candidate for developing therapeutic strategies for handling inflammatory diseases.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"414-427"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622817","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":"Alpha7 nicotinic acetylcholine receptor participates in the effect of dexmedetomidine on Treg cell differentiation.","authors":"Yulan Wang, Xiaoyan Yang, Xiaoqi Kong, Huanle Gong, Yishan Lei, Fuhai Ji","doi":"10.1080/08923973.2026.2640188","DOIUrl":"10.1080/08923973.2026.2640188","url":null,"abstract":"<p><strong>Background: </strong>The anti-inflammatory effect of dexmedetomidine can be mediated through alpha7 nicotinic acetylcholine receptor (α7nAChR). However, it remains unknown whether α7nAChR is involved in mediating the effects of dexmedetomidine on CD4⁺T cell differentiation. The study aims to explore whether dexmedetomidine can affect CD4⁺T cell differentiation through α7nAChR.</p><p><strong>Methods: </strong>Naïve CD4⁺T cells obtained from mouse spleens were incubated with different concentrations of dexmedetomidine for 3 days <i>in vitro</i>. The percentages of helper T (Th)1, Th2, Th17, and regulatory T (Treg) cells were determined by flow cytometry. The corresponding transcription factors T-bet (Th1), GATA-3 (Th2), ROR γt (Th17), and Foxp3 (Treg) were detected using quantitative real-time PCR. Mice with tibia fracture were pretreated with dexmedetomidine or methyllycaconitine (MLA, an α7nAChR antagonist) for 48 h <i>in vivo</i>. The percentages of Th1, Th2, Th17, and Treg cells were determined. Naïve CD4⁺T cells were incubated with dexmedetomidine and MLA <i>in vitro</i> and Treg cells were detected. The level of interleukin (IL)-10 secreted by Treg cells was quantified by an enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>Dexmedetomidine administration, both <i>in vitro</i> and <i>in vivo</i>, suppressed Th1 cell differentiation along with its transcription factor T-bet, while promoting Treg cell differentiation and upregulating Foxp3. Conversely, MLA reversed these effects of dexmedetomidine on Th1 and Treg cell differentiation <i>in vivo. In vitro</i>, MLA also attenuated the dexmedetomidine-induced enhancement of Treg cell differentiation and the associated IL-10 secretion.</p><p><strong>Conclusion: </strong>Dexmedetomidine promotes Treg cell differentiation while inhibiting Th1 cell differentiation. This regulatory activity on Treg cells may be mediated through the α7nAChR pathway.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"282-291"},"PeriodicalIF":3.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365154","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":"Implications of inflammasomes in dental pulp inflammation: immunopathology and therapeutic targeting.","authors":"Mohammad Javad Yousefi, Kiarash Saleki, Yashmin Afshar, Nima Rezaei","doi":"10.1080/08923973.2026.2625040","DOIUrl":"10.1080/08923973.2026.2625040","url":null,"abstract":"<p><strong>Objectives: </strong>Pulpitis is a dynamic condition that affects vascular and immune responses. A major driver of inflammation is the inflammasome, which regulates interleukin-1 (IL-1) family cytokines and pyroptosis. Pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) activate the inflammasome via caspase recruitment, which is essential for the inflammasome's immunomodulatory effects.</p><p><strong>Materials: </strong>In order to synthesize evidence for this review, a comprehensive search was conducted in PubMed, Scopus, and Web of Science. Subsequently, preclinical models and clinical studies on the role of inflammasome components in dental pulp inflammation were selected and critically presented.</p><p><strong>Results: </strong>According to recent research, factors associated with the inflammasome are dysregulated during dental pulpitis, while therapeutic targeting through computational discovery of anti-inflammasome ligands and cell-free exosome-based treatments can counteract the immunopathology of dental pulpitis.</p><p><strong>Conclusion: </strong>Although preclinical studies were promising, comprehensive clinical trials of IL-1 family and inflammasome inhibitors are required for translating current research into viable treatments for patients with dental pulpitis. Future work should prioritize clinical validation to enable implementation in patient care.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"292-302"},"PeriodicalIF":3.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467896","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":"Galantamine supplementation and rheumatoid arthritis: a systematic review of current research and molecular mechanisms.","authors":"Niloufar Orooji, Fatemeh Ahmadi, Zeinab Javadivala, Aida Malek Mahdavi, Mehdi Jafarpour","doi":"10.1080/08923973.2026.2635989","DOIUrl":"10.1080/08923973.2026.2635989","url":null,"abstract":"<p><strong>Objective: </strong>Rheumatoid arthritis (RA) is a chronic inflammatory disease that can cause serious joint destruction if not properly managed. Despite established treatments, many patients struggle to find meaningful relief, emphasizing the need for new treatments. Galantamine (GAL), a naturally occurring alkaloid and acetylcholinesterase inhibitor with anti-inflammatory effects, has showed promise in preclinical RA research.</p><p><strong>Methods: </strong>This systematic review assessed GAL's potential in RA by searching PubMed, Scopus, ISI Web of Science, and Google Scholar until June 2025, with no language or date restrictions. We omitted review articles, conference abstracts, book chapters, and studies that combined GAL with other substances or diseases. There was no human or <i>in vitro</i> research found, so seven eligible animal studies were analyzed.</p><p><strong>Results: </strong>Evidence suggests that GAL improves RA outcomes by lowering inflammation and oxidative stress, blocking angiogenesis, and exhibiting anti-arthritic effects. These findings imply that GAL could be an effective treatment for RA. However, the available evidence is limited to animal models, and well-designed clinical trials are required to prove its efficacy and safety in people.</p><p><strong>Conclusion: </strong>This review emphasizes GAL's therapeutic potential as well as the critical need for translational research to bridge the gap between preclinical and clinical applications.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"224-233"},"PeriodicalIF":3.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283770","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}