Inflammopharmacology最新文献

{"title":"The immunoproteasome in Alzheimer's disease: a dual regulator of tau pathology and microglial senescence.","authors":"Mustafa M Shokr, Ahmed M Abdelaziz","doi":"10.1007/s10787-026-02393-1","DOIUrl":"https://doi.org/10.1007/s10787-026-02393-1","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is characterized by progressive cognitive decline driven by the convergence of tauopathy, impaired proteostasis, and chronic neuroinflammation. Emerging evidence identifies the immunoproteasome (iP), particularly the β5i/LMP7 subunit, as a central regulator linking these pathological processes. Unlike the constitutive proteasome, the iP is markedly induced in microglia, neurons, and astrocytes under inflammatory conditions through interferon-γ and NF-κB signaling. This review discusses the dual and context-dependent role of the iP in AD pathogenesis. In microglia, chronic iP activation promotes degradation of NRF2, leading to oxidative stress, NLRP3 inflammasome activation, and the development of a senescence-associated secretory phenotype that exacerbates neuroinflammation and tau propagation. In neurons, moderate iP activity facilitates the clearance of phosphorylated tau; however, sustained overactivation generates aggregation-prone tau fragments that enhance trans-synaptic tau spreading. We further highlight the cross-talk between the iP and autophagy pathways through TFEB and p62/SQSTM1 signaling and discuss how gut microbiota-derived inflammatory mediators may prime central iP activation through the gut-brain axis. Importantly, recent preclinical studies support the concept of partial immunoproteasome modulation rather than complete inhibition, with selective LMP7 targeting restoring proteostatic balance, reducing microglial senescence, and attenuating tau pathology. Collectively, the iP emerges as a promising immunopharmacological target and a potential therapeutic rheostat in AD.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109084","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":"Curcumin as a natural therapeutic agent for osteoarthritis: molecular mechanisms, preclinical evidence, clinical applications, and future perspectives.","authors":"Nalina Viswanathan, Vidhyavathi Ramasamy","doi":"10.1007/s10787-026-02390-4","DOIUrl":"10.1007/s10787-026-02390-4","url":null,"abstract":"<p><p>Osteoarthritis is a prevalent and progressive musculoskeletal disorder characterized by a complex interplay of mechanical stress, low-grade inflammation, oxidative stress, extracellular matrix degradation, chondrocyte dysfunction, and subchondral bone remodeling. Current pharmacological and surgical approaches primarily provide symptomatic relief and have limited capacity to modify the underlying structural progression of the disease. Curcumin, a major bioactive polyphenol derived from Curcuma longa, has attracted considerable interest as a potential therapeutic candidate because of its ability to influence multiple interconnected pathways involved in osteoarthritis pathogenesis. Unlike many phytochemicals investigated primarily through single mechanistic targets, curcumin has been extensively studied for its coordinated effects on inflammatory signaling, oxidative stress, apoptosis, extracellular matrix turnover, and cellular homeostasis. This review critically examines the molecular mechanisms, preclinical evidence, clinical findings, pharmacokinetic limitations, and emerging delivery strategies associated with curcumin in osteoarthritis. Particular emphasis is placed on the relationship between curcumin's multitarget pharmacology and its translational limitations, including poor aqueous solubility, low systemic bioavailability, rapid metabolism, variability among formulations, and heterogeneity of clinical studies. Evidence from experimental models supports anti-inflammatory, antioxidant, chondroprotective, and tissue-preserving effects, whereas clinical studies mainly indicate potential benefits for pain and functional outcomes. However, current evidence remains insufficient to establish curcumin as a disease-modifying therapy. Recent advances in nanotechnology, lipid-based systems, targeted delivery, and curcumin analogues may improve exposure and therapeutic efficacy, although their clinical translation remains to be established. Overall, curcumin represents a biologically plausible multitarget candidate for osteoarthritis, but larger, well-designed, standardized clinical trials incorporating structural and molecular endpoints are required to determine its therapeutic and disease-modifying potential.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6363-6388"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148880011","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 cytokine-driven neuroinflammation in Alzheimer's disease: mechanistic insights and pharmacological strategies.","authors":"Rufaida Wasim","doi":"10.1007/s10787-026-02342-y","DOIUrl":"10.1007/s10787-026-02342-y","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the most common neurodegenerative disorder and the leading cause of dementia worldwide. Although the classical pathological hallmarks of AD include extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein, increasing evidence indicates that neuroinflammation plays a central role in disease initiation and progression. Among the key mediators of neuroinflammatory responses, cytokines have emerged as critical regulators of immune communication within the central nervous system. Activated microglia and reactive astrocytes release a wide range of pro-inflammatory cytokines, including IL-1β, IL-6, TNF-α, and interferon-γ, which contribute to synaptic dysfunction, neuronal injury, and amplification of inflammatory signaling pathways. Conversely, anti-inflammatory cytokines such as interleukin-10, interleukin-4, and transforming growth factor-β participate in regulating immune homeostasis and may exert neuroprotective effects by suppressing excessive inflammatory responses. This review provides a comprehensive overview of cytokine-mediated neuroinflammation in Alzheimer's disease, focusing on the cellular sources of cytokine production within the brain, including microglia, astrocytes, neurons, and endothelial cells. Key intracellular signaling pathways involved in cytokine activity, such as nuclear factor-κB (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK-STAT), and mitogen-activated protein kinase (MAPK) pathways, are also discussed in relation to their roles in inflammatory amplification and neurodegeneration. Furthermore, the complex interactions between cytokine signaling, amyloid-β accumulation, and tau pathology are examined to highlight the interconnected mechanisms underlying disease progression. Finally, emerging therapeutic strategies targeting cytokine-driven neuroinflammatory pathways are explored, emphasizing their potential in the development of novel anti-inflammatory and disease-modifying treatments for Alzheimer's disease.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6487-6517"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891251","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":"Design, development, and optimisation of an amorphous solid dispersion-based etoricoxib bigel for targeted topical anti-inflammatory drug delivery.","authors":"Jitendra W Gajbe, Ashwini R Madgulkar, Bandenawaz M Shaikh, Mangesh R Bhalekar, Sejal A Tawari","doi":"10.1007/s10787-026-02384-2","DOIUrl":"10.1007/s10787-026-02384-2","url":null,"abstract":"<p><strong>Background: </strong>Etoricoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, exhibits limited aqueous solubility that restricts its therapeutic performance in topical delivery systems.</p><p><strong>Purpose: </strong>This study aimed to develop and evaluate a novel bigel-based topical delivery system incorporating pure etoricoxib and etoricoxib-loaded amorphous solid dispersion (ASD) to enhance solubility, stability, and anti-inflammatory efficacy, with an improved onset of action.</p><p><strong>Study design: </strong>A Box-Behnken experimental design was employed to optimise the bigel formulation by evaluating the effects of organogelator concentration, hydrogelator concentration, and ASD percentage on viscosity, hardness, and time required for 50% drug release.</p><p><strong>Methods: </strong>Bigels were prepared by blending hydrogel and oleogel phases at different ratios. The formulations were characterised for physical appearance, pH, spreadability, viscosity, and drug content. Further evaluation included rheological studies, in vitro release, and ex vivo skin permeation assessments. Dermal safety was evaluated using a skin irritation model, and anti-inflammatory activity was investigated using a carrageenan-induced paw oedema model in animals.</p><p><strong>Results: </strong>Compatibility studies confirmed the absence of any significant interaction between etoricoxib and excipients. Carbopol 940 and stearic acid, in an 80:20 ratio, were identified as the optimised hydrogelator and organogelator, respectively. The statistical model best fitting the data was a second-order interaction (2FI) model. Increasing concentrations of hydrogelator and organogelator resulted in higher viscosity and hardness, whereas an increased proportion of ASD significantly enhanced drug release. The optimized formulation achieved ~ 80% drug release within 8 h. It showed enhanced etoricoxib permeation, with Jss (14.816 µg/cm²/h) and Kp (0.004 cm/h) exceeding the marketed formulation (11.76 µg/cm²/h and 0.003 cm/h, respectively). The optimized bigel demonstrated good dermal tolerability and significantly reduced paw edema in vivo.</p><p><strong>Conclusion: </strong>The developed bigel formulation exhibited favourable physicochemical and biopharmaceutical properties, indicating strong potential as an effective topical delivery system for the management of pain and inflammation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6643-6661"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989890","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":"Evaluation the role of quinoa seeds in attenuation the brain cellular senescence and aging induced by D-galactose and γ-radiation in rats: insights into autophagy, telomerase activity, amyloid-β and tau proteins.","authors":"Merehan Alaa-ElDin Mohamed, Mustafa M M Elbakry, Nermeen M Elbakary, Said S Moselhy, Youssef A Said","doi":"10.1007/s10787-026-02377-1","DOIUrl":"10.1007/s10787-026-02377-1","url":null,"abstract":"<p><p>The gradual loss of cognitive function, manifested by impaired learning and spatial memory, is a hallmark of brain senescence during aging. However, effective natural interventions targeting multiple mechanisms involved in aging-related neurodegeneration remain limited. This study assessed the possible protective efficacy of quinoa seed powder (QSP) against D-galactose (D-gal)- and γ-radiation-induced brain senescence in rats. Fifty male albino rats (n = 10/group) were randomly allocated into five experimental groups. Aging was induced by D-gal administration and fractionated whole-body γ-radiation (1.5 Gy/week for four consecutive weeks; total dose 6 Gy). Behavioral performance, oxidative stress biomarkers, telomerase activity, autophagy markers, neurodegenerative proteins, histopathological alterations, antioxidant activity of quinoa ethanolic extract (QEE), and molecular docking were evaluated. QSP significantly (P < 0.05) attenuated oxidative stress, as evidenced by decreased malondialdehyde levels and increased catalase activity and reduced glutathione content. Furthermore, QSP significantly reduced amyloid-β 1-42 (Aβ42) and Tau protein accumulation, increased telomerase activity, and enhanced autophagy-related modulation through upregulation of microtubule-associated protein 1 light chain 3 beta (LC3B) and downregulation of mammalian target of rapamycin (mTOR) expression. In vitro analysis showed that QEE exhibited potent antioxidant activity, with EC50 values of 16.67 and 23.01 mg/mL for TAC and FRAP, respectively, and an IC₅₀ value of 5.91 mg/mL against DPPH radicals. Docking analysis showed that kaempferol exhibited the most favorable binding affinities among the tested quinoa constituents toward mTOR (- 7.579 kcal/mol) and catalase (- 7.286 kcal/mol), with short-timescale molecular dynamics analyses providing additional structural support for the predicted interaction profiles. These findings suggest that QSP exerts multi-target neuroprotective effects through attenuation of oxidative stress and modulation of autophagy-related pathways, supporting its potential as a natural strategy for mitigating aging-associated neurodegenerative changes.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6819-6838"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13675366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149008422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological modulation of cGAS-STING-NLRP3 signaling by nano-immunomodulators in Alzheimer and Parkinson disease.","authors":"Mohammed A Abdel-Rasol","doi":"10.1007/s10787-026-02386-0","DOIUrl":"10.1007/s10787-026-02386-0","url":null,"abstract":"<p><p>Neuroinflammation is a central driver of neurodegeneration in Alzheimer's disease (AD) and Parkinson's disease (PD), driven by interconnected pathways involving microglial state dysregulation, inflammasome activation, cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling, impaired mitophagy, CD33-TREM2 imbalance, gut-brain axis disruption, and peripheral immune infiltration across a compromised blood-brain barrier (BBB). Conventional anti-inflammatory therapies remain limited by poor CNS delivery, inadequate cell specificity, and the inability to simultaneously modulate multiple inflammatory pathways. Nano-immunomodulators (NIMs) have emerged as a promising strategy to modulate CNS immunity in preclinical models. This review critically evaluates recent advances in NIM-based strategies for AD and PD, including intrinsically therapeutic nanomaterials, targeted delivery systems, and precision gene-regulatory platforms. Intrinsically therapeutic materials, such as polydopamine nanoparticles and biomimetic nanozymes, provide antioxidant and mitochondrial protective functions, whereas BBB-targeted systems, including nanobody-based platforms and engineered exosomes, enhance targeted CNS delivery. Nanotheranostics approaches integrate imaging capabilities with stimuli-responsive release, while precision interceptors aim to simultaneous regulate pathological processes such as amyloid-beta (Aβ)-associated inflammation and cGAS-STING activation. Emerging gene-delivery strategies, including TREM2 mRNA and CD33-targeting lipid nanoparticles, offer opportunities for microglial reprogramming but remain largely restricted to proof-of-concept and early preclinical stages. The review further discusses AI-driven nanomedicine optimization and advanced human-relevant models, including brain-on-a-chip systems and three-dimensional (3D) bioprinting, as tools to improve translational prediction. Currently, AI approaches primarily support candidate selection, formulation optimization, and mechanistic prediction rather than clinical validation. Major challenges for clinical advancement include achieving precise modulation of microglial states beyond the simplified M1/M2 framework, developing context-dependent regulation of NLRP3 and cGAS-STING pathways, establishing gut-CNS therapeutic strategies, improving pluripotent stem cell (iPSC)-based validation platforms, and defining long-term CNS safety frameworks. By integrating molecular mechanisms, AI-assisted nanomedicine, nanoparticle-enabled immune and gene modulation, and advanced preclinical models, this review provides a mechanistic and translational framework for advancing next-generation NIM strategies in AD and PD. This integrated perspective addresses the limitations of previous single-domain analyses focused either on neuroinflammation or nanotechnology and outlines key considerations for translating NIMs from experimental platforms toward clinical applications.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6451-6485"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13675331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obeticholic acid attenuates complete freund's adjuvant-induced arthritis in rats through FXR-mediated modulation of TGF-β/TAK1/MKK3/p38 MAPK signaling, inflammation, and oxidative stress.","authors":"Mohamed Magdy Senna, Nesma A Shiha, Hala F Zaki, Laila A A Ramadan, Aya M Mustafa","doi":"10.1007/s10787-026-02389-x","DOIUrl":"10.1007/s10787-026-02389-x","url":null,"abstract":"<p><p>Rheumatoid arthritis is a chronic autoimmune inflammatory disorder characterized by synovial inflammation, oxidative stress, cartilage destruction, and progressive joint damage. Farnesoid X receptor activation has recently emerged as a potential regulator of immune and inflammatory responses. This study investigated the effect of obeticholic acid (OCA), a potent farnesoid X receptor agonist, in a complete Freund's adjuvant-induced arthritis model in rats, with emphasis on the TGF-β/TAK1/MKK3/p38 MAPK signaling pathway, inflammatory mediators, and oxidative stress.Arthritis was induced in male Wistar rats by subplantar injection of complete Freund's adjuvant on days 0 and 7. Rats were allocated into nine groups: normal control, OCA control, arthritic control, arthritic rats treated with OCA at 2.5 or 5 or 10 mg/kg, methotrexate-treated arthritic rats, F44-A13-treated arthritic rats, and arthritic rats co-treated with F44-A13 and OCA. Treatments were administered orally from day 8 for 14 consecutive days. Clinical arthritis severity, paw edema, pain behavior, body weight, immune organ weight, serological markers, inflammatory cytokines, oxidative stress markers, gene expression, and histopathological changes were evaluated.Obeticholic acid significantly ameliorated arthritic manifestations, as evidenced by reduced arthritis score, paw swelling, pain behavior, spleen and thymus weight, and improved body weight. It also decreased serum rheumatoid factor, C-reactive protein, and anti-cyclic citrullinated peptide levels. Obeticholic acid treatment was associated with restoration of FXR expression and downregulation of TGF-β, TGF-βR1, TAK1, MKK3, and p38 MAPK expression, accompanied by suppression of NF-κB, TNF-α, IFN-γ, IL-1β, and IL-6. In parallel, obeticholic acid enhanced antioxidant defenses by increasing Nrf2, superoxide dismutase, and catalase while reducing malondialdehyde levels. Histopathological assessment confirmed attenuation of synovial inflammation, cartilage damage, and proteoglycan loss. Co-administration of the FXR antagonist F44-A13 markedly blunted the protective effects of obeticholic acid.These findings indicate that OCA attenuates CFA-induced experimental arthritis and that these effects are associated with FXR-related changes in TGF-β/TAK1/MKK3/p38 MAPK gene expression, inflammatory mediators, and oxidative stress.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6679-6696"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13675349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acitretin shows promising potential in Alzheimer's disease: retinoid-driven modulation of amyloid processing, neuroinflammation, and translational prospects.","authors":"Varun Sharma, Kanika Vashisht, Garima Choudhary, Vaishali Choudhay, Vandana Bhatia, Mahendra Singh Ashawat, Ashish Baldi, Shiv Kumar Kushawaha","doi":"10.1007/s10787-026-02392-2","DOIUrl":"10.1007/s10787-026-02392-2","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder driven by the convergence of amyloid-β (Aβ) accumulation, tau hyperphosphorylation, synaptic failure, and chronic neuroinflammation, for which effective disease-modifying therapies remain elusive. Increasing evidence identifies dysregulated retinoid signaling as a critical yet underexplored contributor to AD pathogenesis. Retinoic acid, acting through retinoic acid receptors (RARs) and retinoid X receptors (RXRs), is essential for maintaining neuronal homeostasis, synaptic plasticity, and neuroimmune equilibrium in the adult central nervous system. In AD, impairment of RAR/RXR signaling shifts amyloid precursor protein (APP) processing toward amyloidogenic pathways, sustains NF-κB-driven inflammatory cascades, and promotes microglial dysfunction, thereby accelerating the progression of neurodegenerative processes. This review integrates mechanistic, preclinical, and translational evidence supporting acitretin, a second-generation synthetic retinoid, as a multi-target therapeutic candidate for AD. Acitretin enhances ADAM10-mediated non-amyloidogenic APP cleavage, increases soluble APP-α production, and reduces Aβ generation in transgenic AD models, while concurrently modulating microglial activation to attenuate pro-inflammatory cytokine signaling, including IL-6 and TNF-α, and preserve synaptic integrity. Importantly, biomarker-based clinical studies demonstrate increased cerebrospinal fluid APP-α following acitretin administration, confirming central target engagement in humans. Although definitive clinical efficacy remains to be established, acitretin's pleiotropic mechanism, established pharmacological profile, and biomarker responsiveness position it as a promising repurposed candidate within biomarker-guided and combination-based therapeutic strategies for AD.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6549-6560"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879998","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":"Modulation of p38 MAPK signaling in spinal cord injury by curcumin: targeting inflammation, oxidative stress, and apoptosis.","authors":"Shokoufeh Rahmani, Arman Gholami Abroumand, Salim Davlatov, Fatemeh Mortazavi Moghadam, Natalia V Kolaeva, Fatemeh Tahmasebi, Hamideh Babaloo, Madjidova Yakutkhon, Kosim Rakhmanov","doi":"10.1007/s10787-026-02405-0","DOIUrl":"10.1007/s10787-026-02405-0","url":null,"abstract":"<p><p>Spinal cord injury (SCI) triggers a complex secondary injury cascade characterized by neuroinflammation, oxidative stress, and programmed cell death, in which p38 mitogen-activated protein kinase (MAPK) signaling has emerged as an important regulatory node. Curcumin, a pleiotropic polyphenol derived from Curcuma longa, has attracted considerable interest as a potential neuroprotective agent because of its anti-inflammatory, antioxidant, and anti-apoptotic properties. Accumulating preclinical evidence suggests that curcumin can modulate p38 MAPK-associated signaling, attenuate inflammatory mediator production, reduce oxidative damage, and improve histological and functional outcomes in experimental SCI. In addition to p38-related effects, curcumin has also been reported to influence interconnected pathways involved in cell survival, gliosis, and stress responses. However, the available literature remains heterogeneous with respect to injury models, formulations, dosing strategies, and outcome measures. Overall, curcumin appears to be a promising adjunctive candidate for limiting secondary injury after SCI, but further mechanistic clarification and improved delivery strategies will be required to enhance translational relevance and support future clinical application.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6389-6412"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024524","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":"Correction: Arbutin mediated neuroprotection in zebrafish model of traumatic brain injury via modulating Nrf2/NF-κB pathway.","authors":"Romanpreet Kaur, Shamsher Singh","doi":"10.1007/s10787-026-02373-5","DOIUrl":"10.1007/s10787-026-02373-5","url":null,"abstract":"","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"6849"},"PeriodicalIF":6.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891335","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}