Cimicifuga and its component actein attenuate acute gouty arthritis by targeting neutrophil activation.

Anti-gout active ingredients from natural plant medicines and their related mechanisms.

The global prevalence of gout continues to rise. Baxian Huazhuo Decoction (BHD) has demonstrated significant efficacy in the clinical treatment of acute gouty arthritis (AGA); however, its mechanism of action remains unclear. This study first employed network pharmacology analysis to identify the key components, targets, and pathways of BHD against AGA. Molecular docking studies validated the binding affinity between the components of BHD and their potential targets. Ultrahigh-performance liquid chromatography-high-resolution mass spectrometry (UHPLC-HRMS) was utilized to identify the active components in BHD and elucidate their fragmentation pathways. Subsequently, a monosodium urate crystal-induced AGA rabbit model was established to evaluate the invivo therapeutic efficacy of BHD. The results revealed 62 predicted active components and 268 target molecules in BHD, identifying core constituents such as gentiopicroside, limonin, and indirubin, which exhibited high affinity for targets including MAPK1, PPARG, and IL-6. Invivo experiments confirmed that BHD significantly suppressed the phosphorylation of MAPK1, reduced the levels of pro-inflammatory factors such as TNF-α and IL-6, mitigated synovial damage, and inhibited the activation of the PI3K-Akt signaling pathway. This study systematically elucidates the pharmacological basis and mechanisms of action of BHD in the treatment of AGA, providing a scientific basis for its clinical application.

Identification of the polyphenols from Lonicera flos-Lonicera Caulis compatibility in gut content and their implication in ameliorating gouty arthritis.

Electroacupuncture alleviates acute gouty arthritis by inhibiting NLRP3 inflammasome activation via modulation of the circadian-inflammation axis.

Fabrication of dissolving PVP/Eudragit microneedles loaded with febuxostat-chitosan nanoparticles for promoting gouty arthritis with hyperuricemia via Nrf2/NF-κB/NLRP3 and VEGF pathways

Connecting the dots: Gouty arthritis, clonal haematopoiesis and myeloid activation, in a unified inflammation model for atherosclerosis progression.

Gallic acid (GA), a plant-derived phenolic compound, is evolving from a general antioxidant into a specific molecular modulator and a functional building block for advanced biomedical materials. This review synthesizes recent insights underpinned by GA's "redox duality"-its capacity to act as either a radical scavenger or a pro-oxidant. In metabolic disorders, GA reprograms cellular machinery by modulating the miR-709/Nrf2 axis, enhancing LDL clearance via LDLR/PCSK9, and targeting the incretin system. In oncology, GA exhibits context-dependent toxicity, acting as a selective pro-oxidant to induce apoptosis and synergizing with tyrosine kinase inhibitors (TKIs), though safety interactions require careful assessment. GA's expanded neuropharmacological profile includes mitigating ferroptosis via GPX4 rescue and acting as a positive allosteric modulator of Kv1.1 channels. It also potently inhibits the NLRP3 inflammasome in gouty arthritis. Beyond traditional pharmacology, recent studies highlight GA's emergence in material science, including the development of GA-based Metal-Organic Frameworks (MOFs) and functional hydrogels for osteoarthritis, kidney stone prevention, and wound healing. Despite broad bioactivity, poor bioavailability remains a significant challenge, necessitating innovative bioactive material design and rigorous clinical validation.

Self-disintegrating electrospun short fibers as intra-articular drug depots for gouty arthritis.

Osteoarticular diseases, including degenerative, inflammatory, genetic, and metabolic subtypes, cause severe physical impairment, psychological distress, and substantial economic burden globally. Current therapies often fail to halt progression or carry significant side effects, highlighting the need for novel interventions. Luteolin, a natural flavonoid with a C6-C3-C6 skeleton and characteristic hydroxyl substitutions, exhibits diverse pharmacological activities, including antioxidant, anti-inflammatory, and anti-apoptotic effects. It modulates key signaling pathways (e.g., NF-κB, MAPK, Nrf2/ARE, PI3K/Akt) to suppress synovial inflammation, inhibit matrix metalloproteinase-driven cartilage degradation, protect chondrocytes from oxidative stress-induced apoptosis, and regulate immune-metabolic dysfunctions. Preclinical studies demonstrate its potential efficacy in major osteoarticular diseases such as osteoarthritis, rheumatoid arthritis, reheumatic arthritis, gouty arthritis, and traumatic arthritis, with therapeutic effects observed in cell and animal models but not yet validated in human subjects. However, translational challenges persist, including low oral bioavailability, poor aqueous solubility, and a severe lack of large-scale, well-designed clinical validation. Future research should focus on advanced delivery systems, rigorous clinical trials, and exploring understudied mechanisms to facilitate its clinical translation. This review summarizes luteolin's therapeutic potential and mechanisms in osteoarticular diseases, providing critical insights for developing natural therapeutics.

The year 2025 marked a significant evolution in the understanding and management of gout, characterised by a growing focus on personalised medicine and multidimensional pathogenetic models.This review provides a comprehensive analysis of the scientific literature published during 2025, highlighting key advancements across several fields. Specifically, we discuss emerging epidemiological trends, such as the rising incidence of early-onset gout, and the integration of artificial intelligence into diagnostic imaging. Groundbreaking genetic studies are explored, identifying early-onset disease as a potentially distinct subset, alongside new insights into the 'gut-kidney axis' and the role of the microbiome in urate homeostasis.Furthermore, this review examines updated pathogenetic mechanisms involving immunometabolic reprogramming and evaluates the latest therapeutic strategies for both gouty arthritis and asymptomatic hyperuricaemia.

Acute gout attacks cause severe pain, and short-video platforms have become patients' primary source of information. However, the quality and reliability of this information are increasingly concerning. This study will systematically evaluate the information quality of gouty arthritis-related content on Bilibili and TikTok video-sharing platforms, along with factors influencing video quality. This study systematically evaluated the quality and reliability of 100 popular gout-related videos each from Bilibili and TikTok. Video quality and reliability were assessed using the global quality score, Modified DISCERN (mDISCERN), JAMA Benchmark Standard, and Hexagonal Radar Schema (HRS) tools. Correlations between video quality and metrics such as likes, comments, saves, and shares were also analyzed. Results showed median scores across 4 metrics on Bilibili: global quality score 3.0 (2.00, 4.00), mDISCERN3..0 (3.00, 4.00), JAMA 3.0 (2.00, 3.00), HRS 5.0 (4.00, 6.00); TikTok's corresponding scores were 3.0 (IQR 3.00-4.00), 3.0 (IQR 3.00-4.00), 3.0 (IQR 3.00-3.75), and 3.0 (IQR 2.00-4.50). Although Bilibili's HRS scores were higher than TikTok's, video quality was generally poor across both platforms. Furthermore, the study found a positive correlation between video length and quality. Increased likes and shares may not always reflect improved video quality, as these metrics can be influenced by the entertainment nature of online videos and may not fully indicate quality. Our research indicates that the health information short videos related to gouty arthritis on Bilibili and TikTok have poor quality, but the videos uploaded by medical professionals are considered reliable in terms of comprehensiveness and content quality. Health information seekers must carefully evaluate the scientific accuracy and reliability of short videos providing medical information on Bilibili and TikTok before making healthcare decisions.

Uric acid is the principal end-product of purine metabolism in man and the primary biochemical requirement for the development of clinical gout is hyperuricemia. Prevalence of gout in women who are in their reproductive age is rare and only a few studies were carried out previously to investigate hyperuricemia in pregnancy. In this study, serum uric acid level was studied in 300 pregnant women attending Turai Yar’adua Women and Children Hospital Katsina. The blood glucose level of the women was also determined to check for gestational diabetes and whether there exist any correlation between blood glucose level and serum urate level. All the women recruited for this study were confirmed to be apparently healthy and were not previously diagnosed with diabetes or gouty arthritis. The results of the study obtained revealed that pregnancy is associated hyperuricemia. An average of 344.23±27.24aµmol/L for 1st trimester, 394.22±12.14aµmol/L for 2nd trimester and 455.40±11.52b µmol/L for 3rd trimester serum uric acid level was observed in pregnant women compared to the standard reference range of 380µmol/L for women. Increased serum uric acid level was observed with increased age of pregnancy; thus highest serum urate levels was observed in the third trimester as compared to the first and second trimesters. No correlation was observed between age of pregnant women and serum urate level or blood glucose level. However, slight correlation was observed between blood glucose level and serum uric acid level in most pregnant women with high blood glucose level suggesting a link between hyperglycemia and hyperuricemia. Findings from this study indicate that women diagnosed with gouty arthritis may risk experiencing gout flares when they are pregnant, particularly in their third trimester. Similarly, diabetic women may likely experience hyperuricemia and possibly gestational gouty arthritis during their pregnancy.

Medial meniscus posterior root (MMPR) tears are more commonly observed in female patients with preexisting osteoarthritis (OA); however, the histopathologic basis for medial root predilection and female predominance remains unclear. (1) Is histopathologic degeneration associated with knee OA that selectively affects the MMPR? (2) Is greater histologic degeneration of the meniscus root insertion observed in female patients compared with male patients? (3) Do patients with varus alignment and severe OA exhibit greater tissue degeneration at the meniscus root insertion? This histologic study analyzed menisci harvested from patients with OA undergoing TKA between August 2024 and July 2025. Patients with a history of prior meniscal surgery, rheumatologic or gouty arthritis, or previous cruciate or collateral ligament injury and those who declined participation were excluded. Of 122 eligible patients, 1% (1) declined, the meniscal root could not be retrieved in 18% (22), and tissue quality was insufficient in 11% (13). The final cohort included 86 patients, yielding 138 posterior meniscal roots: 69 MMPR and 69 lateral (LMPR). Of those, 63% (54) of patients were female. Mean ± SD age did not differ between the MMPR and LMPR groups (72 ± 7 versus 73 ± 7 years; p = 0.28). The severity of OA, assessed by Kellgren-Lawrence (KL) grade, was similarly distributed (MMPR Grade III 35% [24 of 69], Grade IV 65% [45 of 69] versus LMPR Grade III 38% [26 of 69], Grade IV 62% [43 of 69]; p = 0.85). Mean ± SD hip-knee-ankle angle was comparable (MMPR 7° ± 6° varus, LMPR 8° ± 6° varus; p = 0.33). American Society of Anesthesiologists (ASA) classification was similar, with 17% of patients with MMPR and 14% of those with LMPR classified as having ASA III, and the remainder as having ASA II. Sagittal root insertions were stained with hematoxylin and eosin and Masson trichrome. Meniscal degeneration was evaluated using the modified Pauli score, a semiquantitative histologic grading system ranging from 0 to 12, with higher scores indicating greater tissue degeneration. Paired comparisons were performed in a subgroup of 52 patients in whom both menisci were analyzed. Linear regression was used to assess associations between histologic degeneration, demographic and clinical variables, and lower-limb alignment within each root group. Histologic degeneration was more severe in MMPRs than LMPRs (mean ± SD modified Pauli score 6.6 ± 2.6 versus 2.7 ± 1.6; p < 0.001), particularly in female patients (6.3 ± 2.5 versus 2.9 ± 2.1; p < 0.001). In 52 patients with paired samples, medial roots again showed more severe degeneration (5.3 ± 2.6 versus 2.2 ± 1.9; p < 0.001), with the shiny white fibers of the medial insertion most severely affected, especially in female patients. A moderately strong correlation was observed between the degree of varus alignment and the severity of MMPR degeneration, with greater varus associated with more severe degeneration (r = 0.54; p < 0.001). After controlling for potentially confounding variables such age, severity of preexisting OA, and lower-limb alignment, we found that male sex was associated with less severe degeneration (β = -2.63 [95% confidence interval (CI) -3.90 to 1.36]; p < 0.001), whereas KL grade IV was associated with more advanced root degeneration (β = 1.87 [95% CI 0.59 to 3.13]; p < 0.001). OA was associated with more severe MMPR degeneration, particularly within the shiny white fibers, with the greatest degree of degeneration observed in female patients with advanced OA and in varus-aligned knees. These OA-related histopathologic changes may contribute to the higher incidence of medial root tears in female patients presenting with preexisting OA and varus malalignment. Moreover, highlighting the histopathologic changes of root insertional degeneration in the presence of additional risk factors may help identify, prevent, and manage MMPR injuries more effectively. These findings may ultimately contribute to improved patient care and long-term success in meniscal root repair.

Pyroptosis is a special form of cell death that often occurs during excessive inflammation and injury, leading to tissue damage, disease progression, and other related issues. The Nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is an important regulatory factor in cellular pyroptosis that promotes the inflammatory response. Inhibitors targeting the NLRP3 inflammasome have emerged as promising potential therapeutic agents for inflammatory diseases. Through large-scale screening, we found that the FDA-approved drug CeeNU strongly inhibited NLRP3-mediated pyroptosis. CeeNU exhibited dose-dependent suppression of NLRP3 inflammasome activation and effectively mitigated inflammasome-driven pyroptotic cell death in both human and murine macrophages/microglia. Mechanistically, we further demonstrated that CeeNU specifically binds to arginine 335 within the NACHT domain of NLRP3, abrogating NLRP3 inflammasome activation by blocking its assembly. Importantly, CeeNU showed remarkable protective effects in multiple mouse models of NLRP3 inflammasome-mediated diseases, including experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG), lipopolysaccharide (LPS)-induced septic shock, monosodium urate (MSU)-induced peritonitis, and MSU-induced gouty arthritis. Our results demonstrate that CeeNU, a clinically available drug, acts as an NLRP3 inhibitor and holds therapeutic potential for NLRP3 inflammasome-mediated pyroptotic diseases.

Background: Gout and chronic lymphocytic leukemia (CLL) represent distinct hematologic and rheumatologic pathologies; however, their concurrent presentation presents significant diagnostic and therapeutic challenges. Tumor lysis syndrome and chemotherapy-induced hyperuricemia are recognized complications of hematologic malignancies, yet the manifestation of acute gouty arthritis with crystallographic confirmation in CLL patients remains an underreported clinical scenario requiring careful diagnostic stratification. Case presentation: We present a 69-year-old male farmer with newly diagnosed CLL (stage C, Binet classification) admitted for acute left knee arthritis with effusion, left ankle arthritis, and concurrent community-acquired pneumonia (CAP). Clinical examination revealed articular inflammation characterized by pain, swelling, erythema, warmth, and significant joint effusion with documented flexion limitation and positive bulging sign. Musculoskeletal ultrasound demonstrated double contour sign, synovial hypertrophy, and effusion measuring 5.8 cm in the suprapatellar recess with monosodium urate (MSU) crystal deposition confirmed by polarized light microscopy of synovial fluid (5,350 cells/mm³, 40% polymorphonuclear neutrophils, 60% mononuclear cells, positive MSU crystals). Serum uric acid was elevated at 10.6 mg/dL. The patient was successfully managed with colchicine, methylprednisolone, arthrocentesis, and supportive care while maintaining CLL treatment preparedness. Conclusion: This case illustrates the importance of confirmatory synovial fluid analysis and ultrasound imaging in the diagnosis of acute gout in the context of hematologic malignancy. Optimal management requires careful coordination between rheumatology and hematology-oncology services to prevent therapeutic complications and ensure safe chemotherapy initiation in CLL patients with concurrent acute gouty arthritis and hyperuricemia.

Smilax glabra Roxb. (SGR) is the dried rhizome of Smilax glabra Roxb., a member of the Liliaceae family. As evidenced by ancient Chinese medical texts, the efficacy of this substance in the elimination of toxins, the eradication of dampness, and the promotion of joint mobility has been well documented. Modern pharmacological studies indicate that it possesses activities such as lowering uric acid, treating gouty arthritis, addressing immune system disorders, and exhibiting antitumor effects. In this paper, chemometric methods were used to construct the spectral effect relationship between the fingerprints of 15 batches of SGR extracts from different origins and varied invitro antigouty arthritis activities. The results showed that the chemical composition of the samples from different sources varied significantly, with the samples from Guangxi, Hunan, and Yunnan provinces exhibiting comparatively higher quality. Among the nine common peaks, neoisoastilbin and isoastilbin were considered to be significantly correlated with the antigouty arthritis activity of SGR. The results of this study will offer reference guidelines for the quality control of SGR, thereby providing a scientific basis for its pharmacodynamic foundation and quality assurance.

The NLRP3 inflammasome, a pivotal component of innate immunity, orchestrates immune defense and inflammatory responses. NEK7, an essential upstream regulator, drives inflammasome assembly through direct interaction with NLRP3. This review systematically summarizes the molecular mechanisms, upstream regulatory networks, and therapeutic targeting of the NEK7-NLRP3 axis. Structurally, NEK7 binds to the leucine-rich repeat (LRR) domain of NLRP3 via its catalytic domain, inducing conformational rearrangement and oligomerization. This structural shift exposes NLRP3's PYRIN domain (PYD), enabling ASC recruitment through homotypic PYD-PYD interactions and subsequent pro-caspase-1 activation to form the mature inflammasome complex. At the regulatory level, cell cycle-dependent NEK7 availability, post-translational modifications (phosphorylation/ubiquitination/palmitoylation), and numerous upstream signals-including kinases, ubiquitin ligases, ionic fluxes, miRNAs, and pathogens-collectively fine-tune the NEK7-NLRP3 interaction. In terms of therapeutic targeting, natural compounds from traditional Chinese medicine (e.g., oridonin, pristimerin), synthetic inhibitors (e.g., MCC950, entrectinib), and biological agents have been shown to suppress inflammasome activation by disrupting the NEK7-NLRP3 interface or modulating associated regulatory pathways. These advances offer novel therapeutic strategies for NLRP3-driven pathologies including gouty arthritis, ischemia-reperfusion injury, neurodegenerative disorders, and metabolic syndromes.

Gouty arthritis (GA) falls within the category of metabolic arthropathies. Its onset stems from abnormal uric acid metabolism, which subsequently leads to the deposition of monosodium urate (MSU) crystals and ultimately triggers a robust inflammatory response. Currently, the global prevalence rate of GA is on the rise, gradually increasing the societal disease burden it imposes. This review comprehensively examines the pathogenesis of GA. The content encompasses uric acid metabolic disorders, the innate immune activation process induced by MSU crystals, as well as various subsequently triggered programmed cell death (PCD) modalities, including pyroptosis, NETosis, apoptosis, necroptosis and ferroptosis. We then evaluate in vivo and in vitro experimental models according to the disease stage and pathogenic processes they best recapitulate. Exogenous MSU models are highly suitable for studying acute inflammatory flares; hyperuricemia models capture the metabolic basis of disease initiation; and composite models more closely reflect the chronic and multifactorial course of human gout. In vitro systems ranging from macrophage monocultures to co-culture and organoid platforms provide complementary tools for mechanistic studies and drug screening. However, current models still cannot fully reproduce the complexity of human gout, particularly with respect to metabolic initiation, tissue hierarchy, systemic context, and species-specific differences. We therefore propose a model-selection approach in which the choice of platform should be guided by the specific pathogenic process under investigation. Future model development should integrate innovative technologies to enhance the authenticity of pathological features, address the shortcomings of existing systems, and facilitate the clinical translation of GA research.

Metabolic diseases represent a significant global public health concern, imposing substantial burdens on healthcare systems, economies, and patient quality of life. Current treatments have limitations, underscoring the need for safer alternatives. Quercetin, a natural flavonoid with favorable human tolerability, shows promise for metabolic disorder management. This review critically evaluates the existing evidence on quercetin's role in metabolic disease management, summarizing its pharmacological advancements and clinical data in treating nine metabolic disorders: diabetes mellitus (DM), metabolic dysfunction-associated fatty liver disease (MAFLD), obesity, atherosclerosis, hyperuricemia, gouty arthritis, hyperlipidemia, osteoporosis, and polycystic ovary syndrome (PCOS). We systematically reviewed studies (2003-2025) from Web of Science, PubMed, Science Direct, and CNKI reporting quercetin's effects in metabolic diseases. Quercetin exhibits multifaceted pharmacological activities, including anti-inflammatory, antioxidant, antiapoptotic, hypolipidemic, and hypoglycemic effects. This underpins its therapeutic potential against nine metabolic disorders. Furthermore, emerging nanodelivery systems have demonstrated enhanced bioavailability, stability, and overall efficacy of quercetin while mitigating its dose-dependent toxicity. Quercetin shows considerable promise in the intervention of metabolic diseases. However, current research lacks mechanistic depth, bioavailability enhancement data, and clinical validation Additionally, clinical studies validating its therapeutic efficacy remain scarce. Further mechanistic investigations and randomized controlled trials are imperative to elucidate quercetin's precise mechanisms and substantiate its clinical potential in metabolic disease management.