Inflammopharmacology最新文献

{"title":"Targeting the cytokine-redox axis: dose-dependent immunomodulation by methotrexate in a biomarker-guided ovine endotoxaemia model.","authors":"Armin Amirian, Aliasghar Chalmeh, Mehrdad Pourjafar, Zahra Akhlaghi Moghaddam","doi":"10.1007/s10787-025-01931-7","DOIUrl":"https://doi.org/10.1007/s10787-025-01931-7","url":null,"abstract":"<p><strong>Background: </strong>Oxidative stress and excessive inflammation are central to the pathophysiology of sepsis and its large-animal analogue, endotoxaemia. Current anti-inflammatory treatments in ruminants lack efficacy in modulating redox balance or acute-phase responses. Low-dose methotrexate (MTX), a known immunometabolic modulator, may offer targeted attenuation of these processes.</p><p><strong>Objective: </strong>To evaluate the anti-inflammatory, antioxidant, and organ-sparing effects of two low-dose MTX regimens in a controlled ovine model of lipopolysaccharide (LPS)-induced endotoxaemia.</p><p><strong>Methods: </strong>20 clinically healthy ewes were randomised into four groups (n = 5/group): Ctrl - (saline), Ctrl + (LPS), LD-MTX1 (LPS + MTX 0.45 mg/kg), and LD-MTX2 (LPS + MTX 0.90 mg/kg). Endotoxaemia was induced via intravenous Escherichia coli O55:B5 LPS, and MTX was administered intramuscularly 1 h post-challenge. Serum biomarkers (TAC, GPx, MDA, haptoglobin, ALT, AST, urea, creatinine and CK-MB), clinical parameters and behavioural scores were assessed at five time points over 24 h. Data were analysed using mixed-effects models with adjusted post hoc contrasts.</p><p><strong>Results: </strong>Both MTX regimens improved TAC within 6 h; LD-MTX2 showed a higher 6 h peak vs Ctrl + (p = 0.0006) and LD-MTX1 increased TAC AUC₀-6 h (p = 0.048). GPx displayed a Group × Time interaction: LD-MTX1 rebounded by 4-6 h, whereas LD-MTX2 recovered later by 24 h. HP was non-monotonic: AUC₀-6 h was lower with LD-MTX1 vs Ctrl + (p = 0.045) but higher with LD-MTX2 vs Ctrl + (p = 0.0002). LD-MTX2 markedly suppressed fever (+ 0.36 °C vs + 1.88 °C in Ctrl + ; p = 0.0011). The organ signals were dose-specific; LD-MTX1 showed no biochemical organ stress, and LD-MTX2 caused transient ALT/AST rises (p ≤ 0.006) with renal indices trending lower and no CK-MB increase. The clinical and behavioural metrics mirrored these effects.</p><p><strong>Conclusion: </strong>Low-dose MTX at 0.45 mg kg⁻¹ produced early redox benefit with partial GPx recovery and lower HP AUC, without biochemical organ stress. The 0.90-mg kg⁻¹ dose improved temperature control and peak TAC but increased HP AUC and caused transient ALT/AST elevations, indicating a narrow therapeutic window. MTX, therefore, warrants evaluation as a precision, time-limited adjunct in early endotoxaemia/sepsis in ruminants, with dose selection guided by time-integrated biomarkers and early liver-enzyme monitoring.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-inflammatory effects of Calebin A on metabolic syndrome via NF-κB signaling pathway modulation.","authors":"Mansuor A Alanazi","doi":"10.1007/s10787-025-01978-6","DOIUrl":"https://doi.org/10.1007/s10787-025-01978-6","url":null,"abstract":"<p><p>Metabolic syndrome is a complex disorder characterized by a combination of events such as insulin resistance, obesity, dyslipidemia, and hypertension, and chronic low-level inflammation plays a major role in its development. The nuclear factor kappa B (NF-κB) signaling pathway plays a critical role in mediating inflammatory responses leading to metabolic dysregulation and progression. Calbin A, a bioactive compound derived from turmeric, exhibited significant anti-inflammatory effects that occur primarily through modulation of the NF-κB pathway. Calbin A is a diarylheptanoid characterized by distinct electrophilic centers that facilitate direct interactions with intracellular signaling molecules, leading to inhibition of NF-κB nuclear translocation and subsequent expression of proinflammatory cytokines. Recent preclinical evidence suggests that Calbin A effectively reduces inflammatory markers, increases insulin sensitivity, and modulates lipid metabolism in both cellular and animal models of metabolic syndrome. Calbin A suppresses NF-κB activation and affects interconnected pathways, including AMP-activated protein kinase and phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), thereby enhancing metabolic homeostasis. These findings suggest that Calbin A may serve as a potential candidate for therapeutic intervention in metabolic syndrome and related disorders. Future research should prioritize comprehensive molecular characterization, increased bioavailability, and clinical translation to effectively utilize Calbin A in the management of metabolic diseases.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antinociceptive, anti-inflammatory, and antiophidic potential of Punica granatum leaves extract and fraction: an in vitro and in vivo evaluation.","authors":"Janaina Carla Barbosa Machado, Joyce Cristina da Silva, Wêndeo Kennedy Costa, Márcia Vanusa da Silva, Alisson Macário de Oliveria, Alessandra Daniele-Silva, Adriana Marina E Silva Parente, Sarah de Sousa Ferreira, Diana Pontes da Silva, Manoela Torres-Rêgo, Felipe França Cavalcanti, Matheus de Freitas Fernandes-Pedrosa, Magda Rhayanny Assunção Ferreira, Luiz Alberto Lira Soares","doi":"10.1007/s10787-025-01934-4","DOIUrl":"https://doi.org/10.1007/s10787-025-01934-4","url":null,"abstract":"<p><p>Punica granatum (Punicaceae) is a shrub with a worldwide distribution that has been used in folk medicine for the treatment of inflammatory disorders. The study investigated the therapeutic potential of spray-dried hydroethanolic extract (SDE) and spray-dried ethyl acetate fraction (EAF) from Punica granatum leaves in models of pain, inflammation, and snakebite envenomation. Phytochemical analysis highlighted the presence of polyphenols, particularly luteolin and hydrolysable tannins in SDE, and a significant concentration of flavonoids in EAF. Both samples demonstrated safety in murine fibroblast cultures, exhibiting no toxicity at concentrations up to 250 µg/mL. In vivo, EAF (25 mg/kg) showed remarkable peripheral antinociceptive activity, reducing abdominal writhings by 88.0%, comparable to morphine (87.0%), and superior to indomethacin (72.0%). In the formalin test, EAF reduced neurogenic and inflammatory pain by 80.9% and 87.3%, respectively, while SDE (200 mg/kg) reduced writhings by 76.7% and inflammatory pain by 57.1%. In the tail immersion test, both extracts increased latency time, confirming central antinociceptive effects. SDE and EAF also reduced carrageenan-induced edema and leukocyte migration by over 70%. In vitro, both samples completely inhibited the proteolytic and hyaluronidase activities of Bothrops brazili and Bothrops leucurus venoms and strongly inhibited PLA₂ activity. Notably, in vivo administration of SDE and EAF significantly reduced B. leucurus-induced paw edema and myeloperoxidase activity by up to 85.5%. These findings reinforce the traditional use of P. granatum leaves and provide the first report of their in vivo analgesic and antiophidic potential, supporting the role of their rich phenolic composition in modulating inflammatory and venom-induced responses.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol: potential therapeutic effects on ocular health.","authors":"Bennett Kurien Biju, Marina Andavar","doi":"10.1007/s10787-025-01947-z","DOIUrl":"https://doi.org/10.1007/s10787-025-01947-z","url":null,"abstract":"<p><p>Resveratrol, a polyphenolic compound predominantly found in grapes and red wine, exhibits significant biological activity due to its potent antioxidant and anti-inflammatory properties. Known for its cardioprotective, chemotherapeutic, neuroprotective, and anti-aging effects, resveratrol has garnered attention for its potential in managing age-related ocular diseases, such as glaucoma, cataract, diabetic retinopathy, and macular degeneration-conditions, where oxidative stress and inflammation play central roles in disease progression and vision impairment. Both in vitro and animal studies indicate that resveratrol impacts key biological pathways, including oxidative stress modulation, inflammation reduction, mitochondrial protection, apoptosis regulation, and angiogenesis suppression, which are implicated in the pathology of these ocular conditions. Resveratrol with antioxidant, anti-inflammatory, and anti-angiogenic properties, shows promise in treating ophthalmic diseases by targeting oxidative stress and abnormal angiogenesis, offering a safer, non-invasive alternative to conventional drugs and better scientific validation than herbal remedies. This review synthesizes current research on resveratrol's mechanisms of action, therapeutic potential, and limitations as a treatment for eye disorders, highlighting its promise as a nutritional intervention and areas requiring further exploration.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dexketoprofen enhances NLRP3 activation via ATPase activity after canonical stimuli.","authors":"Daniel Boy-Ruiz, Juan Miguel Suarez-Rivero, Inés Muela-Zarzuela, Mario D Cordero","doi":"10.1007/s10787-025-01928-2","DOIUrl":"https://doi.org/10.1007/s10787-025-01928-2","url":null,"abstract":"<p><p>Inflammasomes are crucial elements of the innate immune system, responsible for triggering inflammation through the activation of caspase-1. Among them, the NLRP3 inflammasome plays a central role in various inflammatory and immune-related disorders. Dexketoprofen (DXK) is a widely used nonsteroidal anti-inflammatory drug (NSAID), although it has not been tested for its effects on the NLRP3 inflammasome pathway. In this study, we explored the influence of DXK on NLRP3 activation and its associated inflammatory responses in human macrophages. Our results showed that even at low concentrations, DXK enhances the release of IL-1β and promotes cell death upon stimulation with LPS and ATP, nigericin and LPS and nigericin, indicating it increases inflammasome activation. Docking and ATPase assays revealed that DXK binds to the NLRP3 NATCH domain, facilitating ATP hydrolysis and NLRP3 activation. Furthermore, treatment with DXK in combination with nigericin further increased IL-1β secretion, while the NLRP3 inhibitor MCC950 reduced the effects of DXK. These findings suggest that DXK amplifies inflammation in macrophages via NLRP3 activation, emphasizing the importance of caution in prolonged use, especially in autoinflammatory diseases where inflammasomes play a significant role.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Limonene alleviated ulcerative colitis via anti-inflammation, anti-oxidation and regulating intestinal microenvironment in vivo and in vitro.","authors":"Wenxiu Xu, Hongbo Wang, Zhenyu Sun, Hui Zhang, Zhijun Zhang, Xiangrong Sun, Jiayu Gu, Yanling Gong","doi":"10.1007/s10787-025-01974-w","DOIUrl":"https://doi.org/10.1007/s10787-025-01974-w","url":null,"abstract":"<p><p>Limonene, a monoterpene naturally abundant in various Citrus fruits, is widely used as a fragrance component and dietary supplement. Ulcerative colitis (UC), a representative inflammatory bowel disease, is characterized by an arising incidence and considerable impact on human health. Although several reports have demonstrated the beneficial effects of limonene on UC, detailed mechanisms remain incompletely understood. In this study, we employed a dextran sulfate sodium (DSS)-induced UC murine model and a lipopolysaccharide (LPS)-stimulated Caco-2 cell model to explore the mechanisms of limonene on UC. The results revealed that limonene significantly decreased disease activity index (DAI) score and alleviated pathological damage in UC mice, exhibiting therapeutic potential for UC. Limonene significantly inhibited interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) while increased superoxide dismutase (SOD) in both DSS-induced UC mice and LPS-induced Caco-2 cells. Furthermore, limonene significantly increased expressions of Zonula occludens-1 (ZO-1), occludin, and claudin-1, thereby enhancing intestinal barrier integrity. Limonene mitigated UC-associated dysbiosis by shifting the gut microbial composition toward that of healthy controls. Specifically, it modulated the microbiota at the phylum, family, genus and species levels, increasing the abundance of anti-inflammatory bacteria while decreasing inflammatory related taxa. Collectively, our in vivo and in vitro results demonstrate that limonene alleviates UC involving in anti-inflammation, anti-oxidation, restoration of intestinal barrier integrity and regulation of the gut microbiota. Future studies are warranted to explore whether gut microbial metabolites contribute to the protective effects of limonene in UC.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting mGluR7 in Parkinson's disease: a novel approach to neuroprotection and synaptic therapies.","authors":"Gursimran Singh, Khadga Raj Aran","doi":"10.1007/s10787-025-01921-9","DOIUrl":"https://doi.org/10.1007/s10787-025-01921-9","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by dopaminergic neuronal loss in the substantia nigra pars compacta (SNPC) and complex motor and non-motor symptoms. Emerging evidence underscores excitotoxic glutamatergic overactivity as a key pathological driver of neurodegeneration, in addition to neuronal loss caused by dopamine depletion. Among the metabotropic glutamate receptors (mGluRs), mGluR7, a presynaptically located G protein-coupled receptor, has gained significant attention due to its unique low-affinity and high-threshold profile, which allows for selective modulation during synaptic hyperactivity while preserving physiological neurotransmission. mGluR7 is a glutamate sensor and inhibitor of glutamate release, modulating excitotoxicity, neuroinflammation, synaptic plasticity, and mitochondrial integrity, which are key features of PD neuropathology. It is highly expressed in basal ganglia loops and glial cells, providing dual-regulatory functionality in neuronal and immune microenvironments. Positive allosteric modulators of mGluR7 represent a potentially exciting group of compounds to increase receptor activity specifically during hyperglutamatergic conditions. In addition to monotherapy, mGluR7 modulators have significant value in the context of combined or stratified therapies, since they enhance dopaminergic therapy and restore synaptic dysfunction. Moreover, current developments in CRISPR-Cas9, RNAi, viral vectors, and nanomedicine offer new arenas to regulate mGluR7 expression and activity with precision. Translating preclinical success into clinical therapies is now feasible with advances in mGluR7-specific PET tracers, biomarkers, and patient profiling. Together, these findings position mGluR7 as a highly promising therapeutic target. This review critically explores the molecular structure, signaling mechanisms, and CNS distribution of mGluR7 by highlighting its role in modulating excitotoxicity, synaptic dysfunction, neuroinflammation, and mitochondrial stress in PD. It also examines the pharmacological development of mGluR7-targeted agents, their preclinical effects on motor and non-motor symptoms, and their potential in combination therapies. Emerging strategies such as CRISPR, RNAi, nanomedicine, and the development of mGluR7-specific biomarkers and imaging tools are also explored to support precision medicine in PD.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The hydroalcoholic extract of the leaves of red mombin (Spondias purpurea L.) is more effective in accelerating ulcer healing than preventing them in rodents.","authors":"Ruan Kaio Silva Nunes, Bruna Longo, Caio Henrique Willrich, Levy Mota da Silva, Luísa Santiago, Thiago Farias de Queiroz Silva, Lucas Matheus Lessa de Olinda, Layla Francielle Pereira, Heloisa Immianovsky Eisendecker, José Roberto Santin, Larissa Benvenutti, Luiza Felipim Corsi, Bianca Priscila Miranda, Hydima Julião Cóta, Larissa Venzon, Tauani Caroline Santos França, Max Vidal-Gutiérrez, Zuleide Maria Ignacio, Walter Antônio Roman-Junior, Luísa Mota da Silva","doi":"10.1007/s10787-025-01915-7","DOIUrl":"https://doi.org/10.1007/s10787-025-01915-7","url":null,"abstract":"<p><p>This study evaluated the anti-ulcer effects of the hydroalcoholic extract from the leaves of Spondias purpurea L. (SPHE). The gastroprotection was assessed using acidified ethanol-induced gastric ulcer in mice given orally with the vehicle, carbenoxolone (200 mg/kg), or SPHE (10-1.000 mg/kg). The extract's healing activity was evaluated using acetic acid-induced ulcers in rats treated with vehicle, omeprazole (20 mg/kg), or SPHE (3-300 mg/kg). Histological and biochemical analyses were done in ulcerated tissue from both models. SPHE antisecretory action was tested in pylorus-ligated rats. The in vitro antioxidant potential was assessed using the DPPH test; its cytotoxicity and proliferative effects were measured in L929 cells. Mass spectrometry analysis was used to determine the extract's chemical profile and the quantification of phenolic compounds in the extract was performed in LCMS. SPHE induced gastroprotection at a dose of 1.000 mg/kg, and this effect was lost in mice treated with NEM, indomethacin, or yohimbine but not L-NAME. SPHE improves the healing of acetic acid-induced ulcers by 69.5% and 83.7% at 10 and 30 mg/kg, respectively. The microscopic examination confirms the healing effect of SPHE. SPHE enhanced PAS-stained mucins, SOD, and GST activities while decreasing MPO activity, and MDA levels in ulcerated mucosa, and scavenged DPPH radicals but did not change the gastric acid secretion. SPHE showed no cytotoxicity and favored fibroblast proliferation. The presence of hibiscus acid, hydroxy citric acid, hibiscus acid glycoside, ellagic acid, and the flavonoids quercetin and rutin were confirmed and quercetin, caffeic acid, p-coumaric acid, gallic acid, and epigallocatechin were quantified. Therefore, SPHE accumulated chemicals with higher gastric healing potential mediated by gastric protective features, specifically antioxidant resources, mucus barrier, and cell proliferation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potentiation of analgesic activity following the complexation of Algrizea minor Sobral, Faria & Proença (Myrteae, Myrtaceae) leaf essential oil with β-cyclodextrin.","authors":"Paulo Henrique Eloi Fernandes, Bruno Oliveira de Veras, Paulo Henrique Andrade do Nascimento Silva, Júlio César Ribeiro de Oliveira Farias de Aguiar, Daniela Maria do Amaral Ferraz Navarro, Maria Tereza Dos Santos Correia, Márcia Vanusa da Silva","doi":"10.1007/s10787-025-01979-5","DOIUrl":"https://doi.org/10.1007/s10787-025-01979-5","url":null,"abstract":"<p><p>Pain is a fundamental biological process; however, its acute manifestation may result in dysregulation and tissue injury. The Myrtaceae family is well known for its diverse pharmacological activities, and Algrizea minor, a species native to Brazil, has traditionally been used for the management of inflammation and pain. The present study investigated the antinociceptive properties of essential oil Algrizea minor (EOAm) and examined whether its complexation with β-cyclodextrin (β-CD) could enhance its pharmacological efficacy. EOAm was obtained by hydrodistillation, yielding 0.57% (w/w), with β-pinene (66.99%) identified as the major constituent. Antinociceptive activity was evaluated using murine models, including the acetic acid-induced writhing and formalin tests. Free EOAm significantly reduced nociceptive behavior in a dose-dependent manner, producing up to 89% inhibition in the acetic acid model. Remarkably, complexation with β-CD further potentiated the analgesic effect, achieving complete inhibition of nociception at the highest dose tested (200 mg/kg). In the formalin assay, both EOAm and its β-CD complex displayed significant efficacy during the neurogenic and inflammatory phases. Partial reversal of the analgesic effect by naloxone indicates the involvement of the opioid system in the underlying mechanism. Overall, these findings demonstrate that EOAm possesses strong antinociceptive activity, which is further enhanced through β-cyclodextrin complexation. This approach not only improves efficacy but also may increase the stability and bioavailability of the essential oil, highlighting the EOAm/β-CD complex as a promising candidate for the development of novel analgesic therapies.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of long non-coding RNAs in the pathogenesis of gastric cancer-induced by Helicobacter pylori.","authors":"Zeynab Marzhoseyni, Foroogh Neamati, Mansoor Khaledi, Mohammad Hossein Haddadi, Aydin Sadeghi, Mina Yekani, Mohammad Yousef Memar","doi":"10.1007/s10787-025-01957-x","DOIUrl":"https://doi.org/10.1007/s10787-025-01957-x","url":null,"abstract":"<p><p>Gastric cancer (GC) remains a significant global health burden with Helicobacter pylori (H. pylori) infection considered a primary risk factor. However, the precise molecular mechanisms of this relationship are still being elucidated. Recent studies have revealed that long non-coding RNAs (lncRNAs) play a crucial role in regulating gene expression, significantly impacting various biological processes, including carcinogenesis. LncRNAs are non-protein-coding transcripts that are over 200 nucleotides long. It has been reported that lncRNAs play a dual role, in promoting or inhibiting cancer progression through intricate molecular pathways in H. pylori-associated GC. The aim of this study was to provide an overview of the role of lncRNAs in the pathogenesis of GC induced by H. pylori. Upregulated lncRNAs such as H19, GClnc1, LINC00152, and PVT1 in H. pylori-infected patients contribute to tumorigenesis by enhancing cell proliferation, migration, invasion, and inflammation. This is often achieved through interactions with oncogenic pathways, stabilization of pro-tumor proteins, or acting as sponges for tumor-suppressive microRNAs. The mechanisms of lncRNA action are diverse, encompassing epigenetic, transcriptional, and post-transcriptional regulation, as well as influencing protein interactions and key signaling pathways, such as Wnt/β-catenin, PI3K/AKT, and NF-κB. Furthermore, lncRNAs are implicated in DNA damage and genomic instability induced by H. pylori, as well as in creating the tumor microenvironment by regulating angiogenesis and immune evasion. This multifaceted involvement positions lncRNAs as promising diagnostic, prognostic, and therapeutic markers for H. pylori-associated GC, warranting further investigation for novel clinical interventions.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}