Inflammopharmacology最新文献

{"title":"Pharmacotherapeutic potential of daidzein: insights into mechanisms and clinical relevance.","authors":"Chinchu Praisthy Lj, Ravi Kushwah, Sachin Dubey, Vipin Kumar, Smita Jain","doi":"10.1007/s10787-025-01891-y","DOIUrl":"10.1007/s10787-025-01891-y","url":null,"abstract":"<p><p>Daidzein, a soy-derived isoflavone, has gained significant attention due to its diverse pharmacological properties, including antioxidant, anti-inflammatory, and estrogenic activities. This review synthesizes current research on daidzein's biological effects, focusing on its role in chronic diseases, such as cancer, osteoporosis, cardiovascular disorders, and neurodegenerative conditions. Mechanistically, daidzein exerts its effects through estrogen receptor modulation, activation of antioxidant pathways, and regulation of inflammatory mediators. Studies have demonstrated its potential in inhibiting cancer cell proliferation, improving bone mineral density, and reducing oxidative stress in cardiovascular diseases. Furthermore, daidzein's neuroprotective effects suggest promise in managing neurodegenerative disorders like Alzheimer's and Parkinson's disease. Despite its therapeutic potential, the bioavailability and metabolism of daidzein remain critical challenges, with interindividual variability influencing its efficacy. Advances in nanotechnology and formulation strategies aim to enhance its bioavailability and therapeutic applications. This review underscores the need for well-designed clinical trials to validate daidzein's efficacy and safety across different populations. Future research should also explore synergistic effects with other bioactive compounds to maximize its clinical utility.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5145-5171"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952204","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: Tectoridin modulates intertwined molecular pathways in metabolic syndrome: insights from network pharmacology, molecular docking, and in vivo studies.","authors":"Ashwini Kumar Mishra, Pravat Kumar Sahoo, Rajesh Singh, Smita Jain","doi":"10.1007/s10787-025-01878-9","DOIUrl":"10.1007/s10787-025-01878-9","url":null,"abstract":"","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5623-5625"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952774","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":"Retraction Note: Glimepiride mitigates tauopathy and neuroinflammation in P301S transgenic mice: role of AKT/GSK3β signaling.","authors":"Mennatallah O Zaki, S El-Desouky, Doaa A Elsherbiny, Mohamed Salama, Samar S Azab","doi":"10.1007/s10787-025-01819-6","DOIUrl":"10.1007/s10787-025-01819-6","url":null,"abstract":"","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5637"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12443931/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540022","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":"Unlocking the molecular pathway of atopic dermatitis: journey so far and roads ahead.","authors":"Sourabh Kumar, Rohit Sharma, Kumari Komal, Dinesh Kumar, Rashmi Ghosh, Manish Kumar","doi":"10.1007/s10787-025-01900-0","DOIUrl":"10.1007/s10787-025-01900-0","url":null,"abstract":"<p><p>Atopic Dermatitis (AD) is a skin-associated disorder involving hyperactivation of inflammatory cascades. The attributing reasons to this include genetic predisposition, environmental factors and immunopathy. At the genetic level, there is an alteration in the filaggrin gene, which leads to impairment in the epidermal integrity. Hence, it makes the skin susceptible to irritants and allergens, causing skin barrier dysfunction, immune hypersensitivity and amplifying antigen penetration. However, at the molecular level the pathways altered in AD include T cell and cytokine pathway, Th2 pathways, IL pathway IL-4, IL-5, IL-13, Th1 pathway, IFN-γ cytokine pathway, Th17 pathway, IL-17 and IL-22 pathway, TGF-β pathway, JAK- STAT pathway, NFkB pathway, MAP2K2/ERK pathway, PI3K/Akt pathway, and Notch pathway. Overall, these events eventually lead to an increase in cytokine storm, keratinocytes proliferation, epidermal hyperplasia, fibrosis, oxidative stress and skin microbial imbalance. The present review highlights the molecular pathways associated with AD and discusses the crosstalk between inflammation, oxidative stress and genetic factors of AD. Moreover, understanding of these intricate pathways is necessary to develop a futuristic intervention to combat AD.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5203-5234"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144872969","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":"Alphonsea elliptica (Hook.f. and Thomson) methanol leaves extract obliterates inflammatory processes in LPS-induced human plasma.","authors":"Ali Attiq, Juriyati Jalil, Sheryar Afzal, Waqas Ahmad","doi":"10.1007/s10787-025-01843-6","DOIUrl":"10.1007/s10787-025-01843-6","url":null,"abstract":"<p><p>In our previous findings, the methanol extract of A. elliptica (MEL) exhibited platelet-activating factor inhibition, indicating possible anti-inflammatory properties. Despite its ethnopharmacological significance, no studies have thoroughly investigated its anti-inflammatory potential. Based on our preliminary findings, we hypothesised that MEL might exert anti-inflammatory effects by modulating key inflammatory mediators, such as prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), and pro-inflammatory cytokines (IL-1β and IL-6). The cytotoxicity of MEL was assessed on peripheral blood mononuclear cells (PBMCs) using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. In vitro, anti-inflammatory activity was investigated in lipopolysaccharide (LPS)-induced human plasma through an enzyme-linked immunosorbent assay (ELISA) and a radioimmunoassay. In addition, the phytochemical profile of MEL was characterised using LC-ESI-MS/MS spectrometry. The extract demonstrated no cytotoxic effects at 20 μg/mL concentrations. MEL exhibited significant anti-inflammatory activity, with notable inhibition of PGE2 (76.18%) and COX-2 (80.12%), as well as pronounced reductions in IL-1β and IL-6 levels, corresponding to 11.6-fold and ninefold decreases at 10 μg/mL, respectively. Concentration-dependent effects were observed, with IC₅₀ values of 4.09, 5.81, 2.12, and 1.97 μg/mL for PGE2, COX-2, IL-1β, and IL-6, respectively. LC-ESI-MS/MS analysis revealed the presence of 30 bioactive compounds, including Gramine, Eruberin B, and Grossamide, which likely contributed to the extract's anti-inflammatory effects. In conclusion, MEL abrogated LPS-induced inflammatory responses in human plasma at non-cytotoxic concentrations, demonstrating its potential as a natural anti-inflammatory agent. Furthermore, this study is the first to report the phytochemical composition of A. elliptica leaves, providing insights into its bioactive constituents and therapeutic potential.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5409-5419"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12443907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144617408","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":"Veratric acid and zinc: a synergistic approach to accelerated wound healing in rats.","authors":"Rumila Afzal, Sidra Kaleem, Aslam Khan, Fareeha Anwar, Umair Ilyas, Alaa S Alhegaili, Mansoor Ali, Sajid Ali","doi":"10.1007/s10787-025-01857-0","DOIUrl":"10.1007/s10787-025-01857-0","url":null,"abstract":"<p><p>Veratric acid, a naturally occurring derivative of benzoic acid present in various plants and fruits, has been reported to possess antioxidant, anti-inflammatory, antimicrobial, and antihypertensive properties. This study was designed to evaluate the effects of veratric acid (VA) and zinc (ZN) on wound healing in rats, assessing their individual (per se) and combined effects to determine the potential for synergistic healing benefits. In an experimental rat model, key variables, including wound closure rate, collagen synthesis, angiogenesis, and inflammation, were assessed in the presence or absence of VA and ZN, both individually and in combination. According to the study's findings, the combination of VA and ZN (10% + 10%) significantly enhances wound healing by promoting collagen synthesis, accelerating angiogenesis (the formation of new blood vessels), and reducing inflammation, thereby facilitating wound closure. The combination of veratric acid and zinc further amplified these effects, indicating a potential synergistic interaction between the two compounds. In the treatment groups, hydroxyproline levels and antioxidant parameters-including catalase, superoxide dismutase, nitric oxide, malondialdehyde, and glutathione-were significantly restored compared to the diseased control group, showing a recovery pattern similar to that of the standard control group. This study aims to provide the therapeutic potential of veratric acid, zinc, and combinations of both. The combination group shows more promising results as compared to their individual effects, indicating synergistic effects. Our data demonstrated a positive effect of the combination group along with the underlying mechanisms, suggesting its clinical potential for wound-healing applications.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5421-5434"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144690091","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":"A systems biology approach reveals dual neurotherapeutic mechanisms of Dioscorea bulbifera in Alzheimer's disease via estrogen signaling and cholinergic modulation.","authors":"Mayank Roy Chowdhury, Sudarshana Deepa Vijaykumar","doi":"10.1007/s10787-025-01872-1","DOIUrl":"10.1007/s10787-025-01872-1","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder marked by cognitive decline, cholinergic dysfunction, synaptic loss, and neuroinflammation. Existing therapies such as Donepezil and estrogen replacement offer only symptomatic relief, failing to address the complexity of the disease due to their reductionist, single-targeted approach. In this study, we employed an integrative systems biology framework to evaluate the neurotherapeutic potential of Dioscorea bulbifera (DB), a core component of the US-patented polyherbal formulation BHD (comprising Bacopa monnieri, Hippophae rhamnoides, and DB), which has shown promising neuroprotective properties in preclinical models. We identified active phytoconstituents of DB-including Emodin, Beta-sitosterol, Diosgenin, Stigmasterol, Diosbulbin B, Jarnol, and Myricetin-and systematically assessed their interaction with Alzheimer's-relevant hub-bottleneck (H-B) genes using molecular docking, gene expression integration, network pharmacology, and molecular dynamics simulations. Our findings delineate a dual mechanistic model of DB's action: (1) an Estrogen Signaling Module centered around ESR1 and its key signaling associates (MAPK1, MAPK8, AKT1, EGFR, PIK3CA, and MAP2K1), forming a tightly interconnected, feedback-regulated pathway modulating memory, synaptic plasticity, neuroprotection, and inflammation; and (2) a Cholinergic Module involving direct inhibition of ACHE, providing rapid symptomatic relief. Molecular docking and dynamic simulations confirmed the strong and stable interactions of DB bioactives with both ESR1 and ACHE, showing comparable or superior stability to reference drugs (Estradiol and Donepezil). Regulatory network analysis revealed that ESR1 is one of the most connected genes in hippocampal-specific PPI networks and is co-regulated by numerous miRNAs and transcription factors. Co-expression analysis identified additional AD-relevant genes (e.g., PIK3R1, MAPK14, PTEN, DHODH, CAV1) involved in synaptic signaling, oxidative stress, and neurogenesis, while TF-miRNA coregulatory nodes such as miR-199a-3p, miR-181a-5p, GATA2, CREB1, and HINFP added further mechanistic layers to DB's network modulation. KEGG and GO enrichment analyses mapped DB-targeted genes to critical AD pathways, including Estrogen signaling, MAPK, PI3K-AKT, TNF, FoxO, and the Alzheimer's disease pathway itself. This multi-targeted, systems-level modulation by DB underscores its potential not only as a neuroprotective nutraceutical-especially for postmenopausal women vulnerable to estrogen loss-but also as a promising adjuvant to standard AD therapies.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5483-5508"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144784250","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":"Therapeutic potential of Boswellia serrata in arthritis management: mechanistic insights into COX-2, 5-LOX, and NFĸB modulation.","authors":"Koleshwar Mahto, Omkar Kumar Kuwar, Aayushi Maloo, Abhishek Kumar","doi":"10.1007/s10787-025-01912-w","DOIUrl":"10.1007/s10787-025-01912-w","url":null,"abstract":"<p><p>Arthritis is a chronic inflammatory disorder characterized by joint pain, stiffness, and progressive cartilage degeneration, significantly impacting patient's quality of life. Current pharmacological treatments, including nonsteroidal anti-inflammatory drugs and corticosteroids, provide symptomatic relief but are associated with adverse effects and limited long-term efficacy. Boswellia serrata, a medicinal plant with a long history of use in traditional medicine, has gained attention for its potential in arthritis management due to its anti-inflammatory, chondroprotective, and immunomodulatory properties. The bioactive constituents, particularly boswellic acids, have been shown to inhibit primary inflammatory pathways including NFĸB, COX-2, and 5-LOX, thereby reducing inflammation and cartilage degradation. Preclinical and clinical studies suggest that Boswellia serrata alleviates pain, improves joint mobility, and slows disease progression with a favorable safety profile compared to conventional therapies. Despite these promising findings, challenges such as limited large-scale clinical trials, variability in extraction methods, and low bioavailability hinder its clinical application. Future research should focus on optimizing formulation strategies, exploring synergistic effects with existing therapies, and conducting high-quality randomized controlled trials to validate its efficacy and safety. In addition, mechanistic studies investigating its molecular targets and interactions with the gut microbiome could provide deeper insights into its therapeutic potential. This review critically evaluates the current evidence on Boswellia serrata in arthritis management, highlights existing research gaps, and discusses future directions for its clinical development. Addressing these challenges will facilitate its integration into mainstream medicine, offering a natural, safer, and potentially more effective alternative for arthritis treatment.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5085-5096"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855138","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":"MicroRNAs in SARS-CoV-2 infection: emerging modulators of inflammation, pathogenesis, and therapeutic potential.","authors":"Mohammad Fayyad-Kazan","doi":"10.1007/s10787-025-01922-8","DOIUrl":"10.1007/s10787-025-01922-8","url":null,"abstract":"<p><p>Since the onset of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), elucidating the molecular regulators of viral pathogenesis and host response has been a critical international research objective. Among these, microRNAs (miRNAs), small non-coding RNAs, that modulate gene expression post-transcriptionally-have emerged as central orchestrators of host-virus interactions. This review exhaustively examines the roles of host-derived miRNAs in SARS-CoV-2 infection, including their roles in viral entry, replication, immune evasion, inflammation, and tissue injury. Dysregulation of certain miRNAs, such as miR-155, miR-146a, and miR-21, has been implicated in disease severity, comorbidities (such as diabetes, obesity), neurological complications, and pregnancy complications. In long COVID (PASC), chronic miRNA changes are linked to persistent inflammation, fibrosis, and cardiometabolic impairment. We emphasize current breakthroughs in miRNA research, including machine learning algorithms for miRNA-based disease stratification, CRISPR-engineered miRNA modulation, exosomal miRNA delivery platforms, and miRNA-adjuvanted vaccines. These advances highlight the potential of miRNAs as diagnostic biomarkers and therapeutic targets. Nevertheless, shortcomings persist in clinical validation, delivery optimization, and tissue-specific miRNA function elucidation. These gaps must be addressed to involve miRNAs in controlling current and future viral infections. This review consolidated differentially expressed miRNAs across disease stages, comorbidities, and clinical settings, providing a valuable resource for translational research and therapeutic innovation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"4895-4910"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952193","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":"Therapeutic potential of alpha-lipoic acid on mitochondrial dynamics, oxidative/nitrosative stress, and histopathological changes in rat ulcerative colitis model.","authors":"İrem Taner, Nur Banu Bal, Saadet Özen Akarca Dizakar, Veysel Bay, Mürşide Ayşe Demirel","doi":"10.1007/s10787-025-01918-4","DOIUrl":"10.1007/s10787-025-01918-4","url":null,"abstract":"<p><p>Ulcerative colitis is a chronic inflammatory disease affecting the gastrointestinal tract. In addition to treatments aimed at healing inflammation and tissue damage, addressing redox imbalance and mitochondrial dysfunction is crucial. The aim of the present study is to investigate the effects of Alpha-Lipoic Acid (ALA), either alone or in combination with mesalamine, on oxidative/nitrosative stress, mitochondrial dynamics, and histopathological changes in a rat model of ulcerative colitis. Rats were divided into Control (C), Ulcerative Colitis (UC), Mesalamine (M), ALA, and Mesalamine + Alpha-lipoic acid (M + ALA) groups. Colitis was induced by intrarectal administration of 4% acetic acid. The disease activity index was the highest in the UC group and the lowest in the M + ALA group among the treatment groups. Macroscopic scores in the UC, M, and ALA groups were significantly higher compared to the C group. The oxidative stress index was the highest in the UC group, with significantly elevated levels compared to the C, ALA, and M + ALA groups. The nitrotyrosine level was also highest in the UC group and significantly elevated compared to the C, M, ALA, and M + ALA groups. Dynamin-related protein 1, Mitofusin-2, and PTEN-induced putative kinase 1 proteins showed significant increases in the UC group compared to the C group. In contrast, these protein levels were significantly reduced in the M + ALA group compared to the UC group. Histopathological scoring in the UC group increased, and ALA administration significantly ameliorated these parameters. Our results indicate that ALA has beneficial effects on increased oxidative stress, impaired mitochondrial dynamics, and altered histopathological scores in the rat colitis model.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5563-5581"},"PeriodicalIF":5.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952196","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}