Search Results (47,848)

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease marked by excessive extracellular matrix (ECM) deposition. Current FDA-approved therapies, such as pirfenidone and nintedanib, offer limited efficacy in halting disease progression. Lysyl oxidase-like 2 (LOXL2) is a key enzyme involved in ECM remodeling and fibrosis. This study investigates Compound #765, a novel indolizine derivative, as a potential LOXL2 inhibitor for IPF treatment. Methods: Compound #765 was synthesized and characterized using spectroscopic methods. Its inhibitory effect on LOXL2 activity was evaluated using LOXL2 enzymatic assays, in vitro fibrosis models with human lung fibroblasts, and in vivo models of pulmonary fibrosis, including bleomycin-treated and TGF-β1-overexpressing transgenic mice. In silico docking studies predicted the binding affinity of Compound #765 to LOXL2. Results: Compound #765 targeted LOXL2 activity and reduced collagen production in lung fibroblasts. In both bleomycin-induced pulmonary fibrosis and TGF-β1-overexpressing murine models, Compound #765 significantly alleviated fibrosis, as indicated by reduced collagen accumulation and inflammatory cell infiltration. The in silico docking studies predicted favorable binding affinity to LOXL2, which was confirmed through in vitro experiments. Importantly, Compound #765 suppressed fibrosis-associated markers in fibroblasts derived from IPF patients, suggesting translational potential. Conclusions: These results demonstrate that Compound #765 functions as a LOXL2 inhibitor with significant anti-fibrotic effects in vitro and in vivo, offering a promising therapeutic approach for IPF and other fibrotic lung diseases. Full article

Background: The absence of disease-modifying treatments for Parkinson’s disease (PD)—a neurodegenerative condition with escalating global incidence—represents a critical unmet medical need. Traditionally utilized for both dietary consumption and medicinal preparations, the fruit derived from Rosa roxburghii Tratt demonstrates a remarkably rich profile of biologically active compounds, with flavonoids, triterpenoids, and organic acids representing the predominant classes. Experimental evidence indicates that these compounds elicit robust antioxidative, anti-inflammatory, and neuroprotective effects, making them promising candidates for neurodegenerative disease modulation. This study aimed to systematically evaluate the neuroprotective effects of Rosa roxburghii Tratt juice concentrate powder (RRJCP) across the preventive, interventional, and therapeutic stages of PD and to elucidate its underlying molecular mechanisms. Methods: Rosa roxburghii Tratt juice was subjected to rotary evaporation concentration and vacuum freeze-drying to obtain the juice concentrate powder. C57BL/6 mice were randomly assigned to three main groups (prevention, intervention, and treatment), each containing subgroups including a normal control, an MPTP model group, low-, medium-, and high-dose RRCJP groups (50, 100, and 200 mg/kg), and a positive control Madopar group, totaling 18 subgroups. A chronic MPTP-induced PD mouse model was established. Motor function was assessed via the open field test, pole test, and wire hang test. Substantia nigra neuronal morphology was examined by hematoxylin and eosin staining. The area of tyrosine hydroxylase (TH)-positive regions was measured by immunohistochemistry. The levels of oxidative stress indicators in serum were measured using biochemical kits. Network pharmacology was employed to predict core targets, and the expression of PI3K/AKT pathway and apoptosis-related proteins was determined by Western blotting. Results: Compared with the MPTP model group, RRCJP (200 mg/kg) significantly increased the total distance traveled in the open field, shortened the pole climbing time, and improved the wire hang score. It attenuated the morphological disorganization and nuclear pyknosis of substantia nigra neurons, increased the TH-positive area and TH protein expression, reduced serum MDA content, and elevated the activities of SOD and GSH-Px. Network pharmacology analysis indicated that the PI3K/AKT signaling pathway was among the core targets. Western blotting results further showed that the juice concentrate powder upregulated the expression of p-PI3K, p-AKT, and Bcl-2, while downregulating Bax and Cleaved Caspase-3 levels, which was consistent with the network pharmacology prediction. Conclusions: RRCJP exerts neuroprotective effects across the preventive, interventional, and therapeutic stages in PD model mice, the mechanisms of which may be associated with activation of the PI3K/AKT signaling pathway, attenuation of oxidative stress, and inhibition of neuronal apoptosis. Full article

Myostatin is associated with inflammatory processes; however, its renal expression and impact on mitochondrial homeostasis during chronic kidney disease (CKD) remain poorly defined. This study investigated whether omega-3 fatty acids (FAs) modulate renal myostatin and mitochondrial integrity under uremic conditions using both in vivo and in vitro models. In rats with adenine-induced CKD, omega-3 FA supplementation attenuated the increase in renal myostatin expression. Uremia was associated with impaired mitochondrial homeostasis, evidenced by decreased peroxisome proliferator-activated receptor gamma coactivator-1 alpha levels and increased dynamin-related protein 1 levels, alongside the upregulation of mitophagy and inflammatory markers. Furthermore, mitochondrial structural damage and reduced mitochondrial DNA (mtDNA) content were observed in uremic kidneys. Omega-3 FA treatment partially reversed these alterations, restored mtDNA levels, and preserved mitochondrial cristae integrity. In vitro, HK-2 cells treated with indoxyl sulfate exhibited increases in myostatin expression and mitochondrial impairment, which were mitigated by eicosapentaenoic acid, docosahexaenoic acid, or their combination. These findings suggest that omega-3 FAs exert protective effects against uremia-induced renal injury by suppressing myostatin and preserving mitochondrial homeostasis, specifically by modulating biogenesis, dynamics, and structural integrity. Consequently, omega-3 FAs may serve as a potential therapeutic strategy with which to preserve mitochondrial homeostasis in patients with CKD. Full article

Purpose: Inflammatory bowel disease (IBD) is a chronic inflammatory disorder strongly associated with intestinal microbial dysregulation. Although 5-aminosalicylic acid (5-ASA) is widely used in the clinical management of IBD, its therapeutic efficacy is often limited. To address this, the present study aimed to develop a bifidobacterium-derived extracellular vesicle-based drug delivery system (B-MVs@5-ASA) to enhance the therapeutic outcomes of IBD. Methods: B-MVs were isolated by PEG precipitation and loaded with 5-ASA via sonication to obtain B-MVs@5-ASA. Their morphology, particle size, zeta potential, and encapsulation efficiency were analyzed using TEM, DLS, and UV spectrophotometry. Cellular uptake, cytotoxicity (LDH and NO assays), and anti-inflammatory effects were assessed in RAW 264.7 and Caco-2 cells. A DSS-induced colitis mouse model was established to evaluate therapeutic efficacy. Cytokines (ELISA), colon histopathology (H&E), tight-junction proteins (IF), and gut microbiota composition (16S rRNA sequencing) were systematically analyzed. Results: B-MVs@5-ASA exhibited a particle size of 104.3 ± 2.81 nm and an encapsulation efficiency of 11.14% ± 3.63%. B-MVs@5-ASA exhibited the strongest anti-inflammatory effect in vitro and most effectively alleviated DSS-induced colitis in vivo, outperforming monotherapies in reducing inflammation, tissue damage, and enhancing barrier integrity. B-MVs@5-ASA further promoted goblet cell regeneration and beneficially modulated the gut microbiota by enriching Akkermansia and suppressing Escherichia, thereby restoring microbial homeostasis. Conclusions: B-MVs@5-ASA provides potent anti-inflammatory and mucosal-protective effects by modulating cytokine balance, enhancing epithelial barrier function, and reshaping gut microbiota. These findings highlight probiotic vesicle-based nanoplatforms as a safe and promising strategy for targeted IBD therapy. Full article

Background: Melatonin has antioxidant and anti-inflammatory properties that may attenuate ischemia-reperfusion injury, but randomized cardiovascular trial data remain inconsistent. Objectives: This study sought to evaluate the association of melatonin supplementation with cardiovascular outcomes across randomized trials. Methods: We performed a systematic review and meta-analysis of randomized trials comparing melatonin with placebo, usual care, or no melatonin in patients with cardiovascular disease. PubMed, Embase, and CENTRAL were searched from inception to 1 January 2026. Random-effects models with Hartung–Knapp–Sidik–Jonkman confidence intervals were used. Prespecified outcomes included left ventricular ejection fraction (LVEF), change in LVEF, troponin, infarct size by cardiac magnetic resonance, heart failure outcomes, inflammatory and oxidative stress biomarkers, and adverse events. Results: A total of 14 randomized controlled trials involving 1027 participants were included. Melatonin significantly improved change in LVEF from baseline to follow-up (mean difference: 3.95 percentage points; 95% CI: 1.70–6.20; p < 0.001), with the most consistent signal in coronary artery bypass grafting studies (mean difference: 4.65 percentage points; 95% CI: 2.56–6.74). Final LVEF was numerically higher with melatonin but not statistically significant. Troponin reduction was not significant. Narrative synthesis suggested lower inflammatory and oxidative stress markers after coronary artery bypass grafting and improvement in heart failure symptoms and quality of life, whereas infarct size findings in ST-segment elevation myocardial infarction were mixed and timing-dependent. Conclusions: Melatonin was associated with improved LVEF change, particularly in coronary artery bypass grafting settings, but benefit was not consistently demonstrated across final LVEF, troponin, or infarct size outcomes. Full article

Neuropsychiatric disorders are characterized by complex etiologies, widespread involvement of brain regions, and pronounced clinical heterogeneity, with core pathological mechanisms closely associated with abnormal activity in deep brain structures and their functional networks. Although current pharmacological therapies and conventional neuromodulation techniques have shown therapeutic benefits in certain conditions, they are generally limited by insufficient stimulation depth or the risks associated with invasive procedures. Temporal interference (TI) electrical stimulation has recently emerged as a non-invasive deep neuromodulation technique that generates low-frequency difference-envelope fields through high-frequency carrier signals, thereby enabling relatively precise modulation of deep brain regions while maintaining favorable safety and tolerability. This technique provides a novel technical pathway for precision intervention in neuropsychiatric disorders. In this review, we summarize the principles and technical characteristics of TI stimulation and highlight its recent applications in mood and stress-related disorders, cognitive impairment and neurodegenerative diseases, movement disorders, addiction, and disorders associated with dysregulated neural excitability. We integrate its potential mechanisms across multiple levels, including neural oscillations, deep–cortical network synchronization, reward and motivational circuits, synaptic plasticity and structural remodeling, excitatory-inhibitory balance, and gene and epigenetic regulation. Current evidence suggests that TI stimulation can modulate electrophysiological activity and may engage molecular and network-level processes relevant to functional improvement, although durable clinical benefits remain to be established. Although clinical translation remains challenged by parameter optimization, interindividual variability, and long-term safety evaluation, advances in computational modeling, multimodal neuroimaging, and closed-loop stimulation strategies are expected to facilitate its development. Overall, TI stimulation represents a promising non-invasive deep neuromodulation approach for mechanistic investigation and precision treatment of neuropsychiatric disorders. Full article

Parkinson’s disease (PD) and acute kidney injury (AKI) are two conditions with increasing prevalence and severe systemic complications and consequences. This research examines the combined neuroprotective and nephroprotective properties of three medicinal plants, Mucuna pruriens (Muc), Moringa oleifera (Mor), and Silybum marianum (SM), in a murine model of PD, AKI, and their comorbid state (PD–AKI), highlighting the role of the PI3K/AKT/mTOR and Nrf2/NF-κB signaling pathways. The mice were grouped as PD, AKI, or PD-AKI, and with or without the herbal pre-treatment, along with their respective controls. Motor impairments were assessed using the rotarod and pole climb assays. Biochemical indicators of renal function, oxidative stress markers, and inflammatory cytokines were quantified in kidney and brain tissues. Assessment of Nrf2, NF-κB, PI3K, AKT, and mTOR expression levels was performed using qRT-PCR. The AKI groups had significant renal impairment (4-fold increase in creatinine and 7.5-fold increase in BUN), oxidative stress (~5.5-fold increase), and increased cytokine levels (~1.5-fold increase), with downregulation of the PI3K/AKT/mTOR (~2-fold decrease) and Nrf2 signaling pathways (~1.8-fold decrease), alongside upregulation of NF-κB (~2.5-fold increase). The PD and PD-AKI groups exhibited significant neuroinflammation (~1.5-fold increase) and redox imbalance (~6-fold increase) in brain tissue, accompanied by motor impairments (1.6 to 4.6-fold decrease). Pre-treatment with Muc, Mor, and SM significantly ameliorated renal impairments (3.5-fold decrease in creatinine and ~5-fold decrease in BUN) and neurological deficits. These findings establish Muc, Mor, and SM extracts as potent, multi-target interventions capable of disrupting the feed–forward cycle of neuro-renal damage. Full article

The rising prevalence of chronic diseases, driven by population ageing, emerging pathogens, and evolving lifestyles, necessitates stronger healthcare systems that integrate effective prevention with timely intervention. Sepsis remains one of the most critical and life-threatening conditions, associated with high incidence, mortality, and morbidity, and frequently progressing to multiple organ dysfunction and septic shock. Early identification is therefore essential to improve patient outcomes. In this work, we propose a rapid and accurate data-driven framework for early sepsis prediction. The framework comprises four stages: data collection, preprocessing, preparation, and classification. Real-world clinical data from 1000 patients are utilized for early risk assessment. Data preprocessing focuses on cleaning and extracting clinically relevant features, followed by data preparation steps including labeling, dataset splitting, class balancing, and feature scaling. Multiple machine learning and neural network models are then implemented, with optimized parameter selection to enhance predictive performance. Finally, a deployment module enables healthcare professionals to leverage the trained models for real-time patient status assessment, supporting timely clinical decision-making. Extensive experimental results demonstrate that the proposed framework achieves fast and accurate discrimination between septic and non-septic patients, outperforming existing state-of-the-art approaches. Full article

Hydrogel-based stem cell therapy uses different stem cells and bioactive molecules for wound healing in the treatment of diabetes and chronic burn wounds by accelerating angiogenesis, collagen deposition, and inhibition of inflammatory responses. Artificial vessels have already been used for patients with cardiovascular diseases, but most of them are polymeric, which can cause thrombosis and restenosis. 3D bioprinting combines cells, growth factors, and biomaterials to create a setting in which cells grow and differentiate into native tissue-like structures. The current study aimed to create a model of blood vessels using collagen and hyaluronic acid hydrogel combined with endothelial and muscle progenitor cells derived from amniotic mesenchymal stem cells using 3D bioprinting. A computer-aided design (CAD) software was employed to create the 3D models of a blood vessel model and printed using a 3D bioprinter with two printheads: one with bioink encapsulating endothelial progenitor cells and the second with bioink encapsulating smooth muscle progenitor cells. The blood vessel constructs were characterized morphologically and structurally by Fourier Transform Infrared (FTIR) Spectroscopy, thermogravimetric analysis (TGA), Scanning Electron Microscopy (SEM), immunohistochemistry, water uptake, and enzymatic degradation. Viability, proliferation, oxidative stress, vascular endothelial growth factor (VEGF) and nitric oxide (NO) production were assessed to demonstrate the cytocompatibility of the blood vessel constructs. Our results showed that collagen–hyaluronic acid hydrogels embedded with stem cells can be used for vascular constructs, meeting the desired requirements of biocompatibility and accuracy in reproducing the model created in the CAD software v1.0. Full article

Background: Graft-versus-host disease (GVHD) is a common severe complication of allogeneic hematopoietic stem cell transplant. The current treatments are limited by steroid toxicity, broad immunosuppression, and the potential suppression of the graft-versus-tumor (GVT) effect. Developing less toxic therapies is an unmet need. We previously showed that systemically infused negatively charged immune-modifying microparticles (IMPs) composed of carboxylated poly-lactic-co-glycolic acid are taken up by inflammatory monocytes via the MARCO receptor, reducing symptoms and improving survival in inflammatory conditions. We hypothesized that IMPs could reduce acute GVHD manifestations. Methods: Acute GVHD was induced in an MHC-mismatched murine transplant model with radiation conditioning. IMPs were infused for five days; outcomes were compared to saline controls. We assessed organ histopathology, immune cell populations in the spleen and intestine, serum cytokine levels, and the GVT effect. Results: IMP-treated mice showed significant improvements in terms of clinical GVHD scores, histopathology, and survival. They had increased regulatory T-cells in the spleen and intestine and decreased colonic inflammatory monocytes and cytokines such as IL-6 and IFN-γ. IMPs were ineffective in MARCO knockout mice, confirming receptor dependence. Importantly, GVT activity was preserved, as evidenced by improved survival in mice with A20 lymphoma treated with IMPs. Conclusions: Systemic IMPs reduce clinical GVHD signs and improve survival, likely by decreasing inflammatory monocytes via MARCO and expanded regulatory T-cells numbers, while maintaining GVT activity. These findings support further investigation of IMPs as a targeted GVHD therapy. Full article

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) that impacts nearly 3 million people worldwide. While the etiology and pathogenesis of MS are not yet fully understood, current evidence suggests that it results from complex interactions between genetic and environmental conditions. Clarifying the autoimmune mechanisms underlying MS remains a central objective in the development of effective therapeutic strategies. Interferon-beta (IFN-$\beta$) is one of the most frequently prescribed disease-modifying treatments for individuals with MS. However, despite its established efficacy, recent studies report that approximately 30–50% of patients exhibit inadequate response to IFN-$\beta$, largely due to genetic variability. Machine learning (ML), a branch of artificial intelligence (AI), employs data-driven computational models to enhance predictive accuracy and classification. In recent MS research, unsupervised learning techniques such as hierarchical clustering and K-means have been applied for classification purposes. However, these methods often fail to yield optimal solutions because they require numerous arbitrary decisions and perform adequately only when datasets contain clusters of similar sizes and lack significant outliers. Fuzzy systems (FSs) are designed to model complex, ambiguous real-world phenomena. In this study, an AI algorithm incorporating a fuzzy system, informed by expert neurologist input, is proposed to enhance the assignment of unknown class labels related to IFN-$\beta$ response in MS patients. Additionally, a genetic algorithm (GA) is introduced to identify optimal solutions within the search space, facilitating hyperparameter optimization of a deep learning (DL) model trained with genetic biomarkers to identify patients likely to benefit from this therapy. Experimental results demonstrate that the fuzzy system achieved $80\%$ classification efficiency, in contrast to $64\%$ with conventional hierarchical clustering. Furthermore, an artificial neural network (ANN) model, with hyperparameters optimized by the GA, achieved an accuracy of 0.8–1.0, surpassing the multi-layer perceptron (MLP), which achieved 0.6–0.8 accuracy using conventional tuning methods. Full article

Micro- and nanoplastics (MNPs) have now been detected in human blood, placenta, and arterial tissue, yet the oral cavity has received strikingly little mechanistic attention despite serving as a primary portal of environmental exposure and a local site of polymer generation from dental and oral-care materials. This narrative review addresses that gap from an environmental microbiology perspective, synthesizing recent literature on periodontal disease, chronic low-grade inflammation, oral biofilms, dental materials, microbial–plastic interactions, and systemic chronic disease risk. Unlike prior reviews, we apply an explicit three-tier evidentiary framework (established, plausible, unproven) that distinguishes what is directly demonstrated from what is biologically plausible but unproven, and we situate the periodontal environment specifically as a particle-retention and inflammatory-amplification niche. The strongest direct oral evidence shows that human dental calculus harbors at least 26 microplastic types, dominated by polyamide (41.4%), polyethylene (32.7%), and polyurethane (7.0%). Polyethylene isolated from calculus induces cytotoxicity, apoptosis, impaired migration, NF-κB activation, and upregulation of IL-1β and IL-6 in human gingival fibroblasts. From a microbiological standpoint, oral organisms actively degrade methacrylate dental polymers, and the degradation products of these polymers reciprocally modulate oral bacterial virulence gene expression. Across experimental systems, MNPs activate oxidative stress, inflammasome signaling, macrophage polarization, and barrier dysfunction, pathways that overlap extensively with periodontal pathobiology. Adjacent environmental microbiology demonstrates that plastic-associated biofilms enhance extracellular polymeric substance production, quorum sensing, pathogen persistence, and antibiotic resistance gene transfer, supporting a plausible but not yet validated oral plastisphere within plaque and calculus. We argue that periodontitis should be reconceptualized as a chronically inflamed particle-processing interface that may increase local MNP retention, cellular reactivity, and systemic inflammatory spillover, with implications for cardiovascular, metabolic, and other chronic disease risk pathways. Current evidence does not yet prove that environmental MNP exposure causes human periodontitis, and that evidentiary boundary is maintained throughout. A priority research agenda is proposed, centered on contamination-controlled subgingival biomonitoring stratified by periodontal status, spatially resolved multi-species biofilm models, polymer source attribution, and longitudinal clinical studies linking oral plastic burden to inflammatory and systemic outcomes. Full article

Preventive health behaviors play a critical role in reducing disease risks and improving public health outcomes, particularly among vulnerable populations such as women in rural communities. However, limited research has explored the determinants of intentions to adopt preventive health behaviors in developing contexts among women in rural communities. This study applies and extends the Theory of Planned Behavior (TPB) to examine these determinants in Algeria. A cross-sectional study was conducted using convenience sampling among 205 women in rural communities aged 20–60 years across five Algerian cities. Data were collected through a self-administered questionnaire and analyzed using hierarchical multiple regression. The results indicate that attitude, subjective norms, and perceived behavioral control have significant positive effects on behavioral intention. The inclusion of health literacy significantly enhances the model’s explanatory power, with higher literacy associated with stronger intentions. In contrast, perceived healthcare discrimination does not have a statistically significant effect. The extended model explains 57.5% of the variance in behavioral intention. These findings underscore the importance of psychosocial and informational factors in shaping preventive health intentions and support the extension of TPB in this context. They also provide practical implications for policymakers and healthcare practitioners to design targeted social marketing interventions aimed at improving preventive health behaviors and reducing health disparities among women in rural communities. Full article

Real-time detection of apple leaf diseases in orchard environments faces ongoing challenges, particularly in preserving fine-grained disease features with limited computing resources. To address these issues, we propose a high-precision lightweight model based on YOLOv10n, called YOLO-ALD. First, we introduce Spatial and Channel Reconstruction Convolution into deeper backbone networks to replace standard downsampling layers and convolutions. This suppresses spatial and channel redundancy caused by environmental noise and optimizes feature representation. Second, we design a new C2f-Faster-SimAM module for the neck network. This module combines the inference efficiency of FasterNet with a parameter-free 3D attention mechanism to adaptively focus on early lesions, effectively distinguishing them from leaf veins without increasing model complexity. Third, in the detection head section, we use the Focaler-ShapeIoU loss function to optimize bounding box regression. It utilizes a dynamic focusing mechanism and geometric constraints to ensure the localization accuracy of irregular shapes and hard-to-detect samples. Experimental results on our self-built dataset covering four specific diseases and healthy leaves showed that, compared with YOLOv10n, the mAP@0.5 of YOLO-ALD reached 92.1%, achieving a 2.1% increase. In addition, the model has an inference speed of 105 FPS, with only 2.1 M parameters and 5.6 GFLOPs. Therefore, YOLO-ALD achieves a good balance between efficiency and robustness, showing strong theoretical potential for resource-constrained mobile agriculture diagnosis. Full article

Background/Objectives: Phillygenin (PHI), a natural lignan derived from Forsythia suspensa, has garnered attention for its potential to alleviate chronic diseases, including chronic colitis, pulmonary fibrosis, and diabetes. Chronic kidney disease (CKD) poses a global health challenge, characterized by high morbidity and mortality rates and associated with a spectrum of secondary complications. In this study, we aim to investigate the therapeutic effectiveness of PHI on CKD and also identify molecular signals by using a unilateral ureteral obstruction (UUO) mouse model and in vitro experiments. Methods: C57BL/6 mice were administered PHI at 50 mg/kg/day to assess its therapeutic effectiveness. In vitro, lipopolysaccharide (LPS) and adenosine triphosphate (ATP) were used to induce pyroptosis, also known as pyroptosis, in renal proximal tubular cells (NRK52E). Results: After PHI treatment for 14 consecutive days, the collagen deposition and extracellular matrix (ECM) accumulation, the expression of oxidative stress response proteins (catalase, superoxide dismutase 2, NADPH oxidase 4, and thioredoxin reductase 1), pro-inflammatory markers (TNF-α and Cyclooxygenase-2(COX-2), and infiltration of neutrophils and macrophages were significantly ameliorated in the UUO mice. Interestingly, the pyroptosis-related proteins (NLRP3/Caspase-1/GSDMD/IL-1β) and cell apoptotic death were also conspicuously relieved after treatment with PHI. Furthermore, PHI administration significantly attenuated the ATP/LPS-induced NF-κB/NLRP3/Caspase-1/GSDMD pyroptosis signal pathway in NRK52E cells. Conclusions: These results demonstrate, for the first time, that PHI treatment ameliorates inflammation and the related pyroptosis via inhibitory regulation of the NF-κB/NLRP3/Caspase-1/GSDMD axis, leading to attenuated renal fibrosis and progressive CKD in UUO mice and in vitro. Our findings suggest that PHI could be a nutraceutical candidate for attenuating CKD progression. Full article