Ankylosing spondylitis (AS) is a chronic inflammatory disorder predominantly affecting the sacroiliac and spinal joints. Emerging evidence indicates that N6-methyladenosine (m6A) RNA modification plays a critical role in inflammatory regulation. Xinfeng Capsule (XFC), a Traditional Chinese Medicine formula (Xin'an medicine), has demonstrated clinical efficacy in alleviating AS-associated inflammation. However, whether XFC modulates AS pathology through m6A-dependent epigenetic mechanisms remains unclear. This study aimed to investigate whether XFC mitigates AS inflammation by regulating the IL-17/NF-κB pathway via m6A modification. Core therapeutic targets were identified by integrating network pharmacology with RNA-sequencing data. The direct interaction between YTHDC1 and LINC01579 was validated using RNA pull-down and dual-luciferase reporter assays. To identify the functional m6A sites, site-directed mutagenesis of two putative m6A motifs (MUT1 and MUT2) in LINC01579 was performed, and the effects of YTHDC1 knockdown were assessed. An in vitro co-culture model comprising AS patient-derived fibroblast-like synoviocytes (FLS) and peripheral blood mononuclear cells (PBMC) was established, alongside an in vivo proteoglycan-induced arthritis (PGIA) mouse model. To verify the underlying mechanism, gain- and loss-of-function experiments were conducted using overexpression plasmids and small interfering RNAs (siRNAs) targeting LINC01579 and YTHDC1. m6A levels were quantified by MeRIP-qPCR. Inflammation and pathway activation were assessed via immunofluorescence, Western blot, and enzyme-linked immunosorbent assay (ELISA). RNA stability was evaluated using actinomycin D assays, while cell migration was measured by scratch assays. Bone destruction was analyzed using micro-CT and histological staining. Additionally, an IL-17 pathway inhibitor (AIN457) and agonist (SR0987) were employed to validate pathway involvement. Bioinformatics and network pharmacology analysis identified LINC01579 as a core gene in AS inflammation and YTHDC1 as an upstream regulator of LINC01579 m6A modification. RNA pull-down assays confirmed the direct binding of YTHDC1 to LINC01579.Functional studies revealed that mutation of the MUT1 site abolished the regulatory effects of YTHDC1 knockdown on inflammatory cytokines (IL-17, IL-6, TNF-α) and LINC01579 expression. XFC was predicted to inhibit inflammation via the IL-17/NF-κB pathway. In vitro, LINC01579 knockdown significantly enhanced the release of inflammatory mediators and activated IL-17/NF-κB signaling. Conversely, YTHDC1 overexpression increased LINC01579 m6A levels, leading to its downregulation. XFC treatment effectively reduced YTHDC1 expression and LINC01579 m6A modification, thereby restoring LINC01579 levels and suppressing IL-17/NF-κB activation. In vivo, XFC ameliorated joint inflammation, bone erosion, and joint space narrowing in PGIA mice. XFC alleviates AS progression by inhibiting YTHDC1-mediated m6A modification of LINC01579, which prevents its degradation and subsequently dampens IL-17/NF-κB pathway activation. These findings highlight a potential epigenetic mechanism underlying the therapeutic effects of XFC in AS.
Circular RNAs (circRNAs) are emerging as key regulators of gene expression, synaptic plasticity, and neuronal function in Alzheimer's disease (AD). Here, we characterize the biological actions of circPDE4B, a highly expressed circRNA markedly reduced in AD. circPDE4B knockdown in neuronal progenitor cells was combined with RNA sequencing to identify regulated pathways. circPDE4B affinity purification identified major protein and micro RNA (miRNA) interactors. Assays of translation and autophagy integrated circPDE4B actions. We found that circPDE4B knockdown inhibited translation through a mechanism mediated by its major interacting protein, gem-associated protein 5. circPDE4B knockdown also decreased mechanistic target of rapamycin and correspondingly enhanced autophagic flux. Consistent with these actions, circPDE4B knockdown strongly attenuated microtubule-associated protein tau pathology in a 3D human assembloid model of tauopathy. Collectively, our findings identify circPDE4B as a regulator of neuronal homeostasis that integrates translation, autophagy, and miRNA pathways, highlighting a potentially important role in the pathophysiology of AD.
Extensive evidence suggests overlapping pathological mechanisms in the brain of individuals with Parkinson's disease dementia, Down syndrome dementia, and Alzheimer's disease. For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). Subsequently, we performed a transcriptomic analysis that corrected for the transcriptional age in the hippocampus of affected individuals, highlighting common underlying pathogenic mechanisms. There were 45 common differentially expressed genes (DEGs), whereas enriched functional terms were related to lysine N-methyltransferase activity and intermediate filament. Co-expression network analysis displayed a module that was significantly downregulated in the non-demented control group only. This module identified EHMT2 and LMNB2 as hub genes, which were also common DEGs. Overall, these findings uncover shared functional insights in the hippocampus, while specifically highlighting EHMT2 and LMNB2 as potential universal biomarkers or disease-altered targets across neurodegenerative dementias.
Adults with Down syndrome (DS) have a greater likelihood of being diagnosed with congenital heart disease (CHD) and may face unique cardiovascular, respiratory, and immunologic health burdens during hospitalization. While CHD survival has improved in recent decades, national data on hospitalization outcomes of patients diagnosed with DS remain limited. The present study aimed to evaluate trends in hospital admissions, inpatient management, and perioperative outcomes stratified by the presence of DS among CHD patients. This was a retrospective cohort of the 2016-2022 National Inpatient Sample. All adult (18-64 years) hospitalizations with a diagnosis of congenital heart disease, were tabulated using previously validated International Classification of Diseases diagnosis codes. Our Primary outcome of interest was in-hospital mortality. Secondary endpoints included temporal trends in admissions, utilization of various cardiac procedures, and length of stay. Of an estimated 54,410 CHD patients hospitalized, 3745 (6.9%) had diagnosis of DS. During the study period, annual CHD admissions increased (nptrend<0.05), while the proportion of those with DS remained stable (6.6% to 6.2%, 2016-2022; nptrend = 0.23). Patients with DS more commonly presented as having hypothyroidism, dementia, chronic obstructive pulmonary disease (all P < 0.05) and less frequently underwent cardiac procedures (7.6 vs 23.2%, P < 0.001). Following risk-adjustment, the presence of DS remained independently associated with greater odds of mortality among all hospitalizations (AOR 2.00, 95%CI 1.40-2.88, P < 0.001). Adults with DS and CHD represent a clinically vulnerable population with higher in-hospital mortality and lower procedural utilization. These findings underscore the need for dedicated care pathways to improve outcomes during medical admissions.
Being on the "down low" (DL) describes men who identify as straight and secretly engage in same-sex encounters while maintaining heterosexual public identities. While the DL phenomenon has been discussed primarily in the context of African American men, Latino men in the United States experience similar patterns of sexual concealment shaped by cultural forces not experienced similarly by other groups. Relatively little is still known about how machismo, familismo, and religious values affect the sexual decisions and health outcomes of Latino men who have sex with men (MSM), and most existing research aggregates Latino MSM with other racial and ethnic minorities without examining their experiences separately. This article applies three theoretical frameworks to the DL among Latino men. The concealment-specific model is used to explore how the act of hiding same-sex behavior produces anxiety, depression, and ongoing self-monitoring, particularly within cultural settings where discovery threatens masculine standing and family belonging. Sexual configuration theory is used to examine why Western categories of gay and bisexual do not fit the way many Latino men understand their own sexuality, especially in cultural contexts where sexual role rather than partner gender defines sexual identity. Syndemic theory is used to examine how conditions such as homophobia, HIV stigma, substance use, poverty, and immigration status interact to worsen health outcomes for this population. The findings of this analysis suggest that DL behavior among Latino men is shaped by the interaction of cultural, psychological, and structural conditions and cannot be understood through any single framework alone. Applied in combination, these theories explain DL behavior among Latino men more fully than established Western approaches. This article is intended to support future empirical research and the development of culturally informed interventions for Latino MSM.
Down syndrome (DS), caused by trisomy 21, confers a near-universal risk for Alzheimer's disease (AD), yet individuals exhibit marked variability in cognitive decline, suggesting the presence of cellular mechanisms that modulate vulnerability and resilience. However, these mechanisms remain poorly defined in the human brain. Here, we integrate matched single-nucleus RNA-seq and ATAC-seq profiles from the prefrontal cortex (PFC) and amygdala (AMY) of age-matched individuals with DS with and without AD (DSAD), enabling direct comparison within a shared genetic background. We identify basal astrocytes in the PFC as a selectively vulnerable cell state in DSAD, characterized by both reduced abundance and coordinated transcriptional and regulatory reprogramming. This state exhibits a shift away from homeostatic support functions, with decreased cytokine signaling and lipid-handling programs, alongside increased steroid- and nuclear receptor-associated activity. Concomitantly, chromatin accessibility profiling reveals reduced engagement of immune- and stress-responsive transcription factor programs, including AP-1, STAT, and BACH families, with linked regulatory perturbations at loci such as ABCA1, DAB2IP, and IL1RAP. Together, these findings define a previously unrecognized astrocyte state marked by epigenetic constraint and diminished responsiveness to stress and inflammatory signals, distinguishing it from classical reactive astrocyte phenotypes. Our results nominate PFC basal astrocytes as a key locus of vulnerability in DSAD and suggest that failure to mount appropriate astrocyte responses, rather than overt activation alone, may contribute to neurodegenerative progression.
Biomaterial implantation can trigger a foreign body response (FBR) that impedes tissue-implant integration. To investigate how implant porosity influences this response, we compared the immune response to subcutaneous implants of microporous annealed particle (MAP) scaffolds and nanoporous hydrogels using mass cytometry, single-cell RNA sequencing, and multiplex cytokine assays. MAP scaffolds promoted vascularization and tissue integration, marked by increased endothelial and regulatory T cells, and reduced proinflammatory immune cells and cytokines. In contrast, nanoporous hydrogels demonstrated enrichment of basophils, natural killer cells, and macrophage populations associated with fibrosis. Transcriptomic and proteomic analyses revealed that MAP scaffolds suppressed activation of the complement-fibroblast-macrophage signaling loop, particularly the C5a signaling crosstalk pathway. This was confirmed using C5-deficient mice, where complement-driven cytokine production was significantly reduced only in nanoporous implants. These findings demonstrate that scaffold porosity modulates immune and complement responses, identifying a key mechanism by which MAP scaffolds reduce FBR and improve biomaterial integration.
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Against the background of global climate change, increasingly severe drought stress exerts a significant impact on plant growth and yield. This study aimed to clarify the leaf anatomical structure, physiology and biochemistry and transcriptome-level metabolic adaptation mechanisms of ancient P. szechuanica to environmental stress. We selected cuttings of ancient P. szechuanica with a diameter of breast-height (DBH) ≥ 1 m and a tree age of 300-500 years as experimental materials. Natural drought stress was applied to investigate the responses of leaf anatomical structure, physiological and biochemical traits, and transcriptome-level metabolic processes of ancient P. szechuanica under drought stress. The results showed the following changes in leaf anatomical structure under drought stress (compared with the control group, the same below): leaf thickness, pith length and palisade tissue thickness decreased by 49.60 %, 20.1 % and 28.68 %, respectively. The thickness of upper and lower epidermis and spongy tissue first increased and then decreased, with final reductions of 53.13 %, 54.26 % and 50.30 %, respectively. Stomatal length and width also decreased, by 15.67 % and 24.26 % respectively. For physiological and biochemical traits, with the prolongation of drought stress, the soluble sugar content decreased significantly by 7.49 %, while the soluble protein content increased significantly by 44 %.At the transcriptome level, significant differentially expressed genes (DEGs) were screened at different drought stages: 3,353 upregulated and 3,161 downregulated DEGs on the day 4 of drought, 5,208 up-regulated and 9,560 down-regulated DEGs on the day 8, and 15,659 up-regulated and 14,870 down-regulated DEGs on the day 12. These DEGs mediated the drought stress response of P. szechuanica via positive up- or down-regulation.
Being overweight and obese are major health concerns worldwide, contributing to lifestyle-related diseases such as hypertension, dyslipidemia, type 2 diabetes, and cardiovascular disease. Increasing physical activity is an effective strategy for weight management. However, earlier step count studies have remained limited to small populations, short-term measurements of 1-2 weeks, and mainly cross-sectional comparisons of average step counts. The effects of long-term step count changes on weight loss remain unclear. This study was conducted to assess the effects of long-term patterns of step counts on weight loss using data from the "Asmile" mobile health app in Japan. We hypothesized that participants with continuously increasing step counts over time would have a higher likelihood of significant weight reduction than participants who show steady or fluctuating patterns, even if their average step counts were similar. We analyzed data of 2778 Asmile users aged 40-74 years with BMI ≥25 kg/m² who underwent a specific health checkup during fiscal years 2019-2023 and who had valid step count records for 10-14 months. Step count trajectories, reflecting long-term trends in physical activity, were classified using a latent class mixed model into four patterns: UP (increasing), FLAT (steady), DOWN (decreasing), and UP/DOWN (increasing then decreasing). Logistic regression was applied to estimate odds ratios for achieving ≥3% weight loss, with step trajectory as the explanatory variable and weight loss as the outcome. Among participants, 1601 (57.6%) were men and 1177 (42.4%) were women, with respective mean ages of 65.8 (SD 7.9) and 64 (SD 8.2) years. Step count trajectories were distributed as 28.5% UP, 36.2% FLAT, 20.1% DOWN, and 15.2% UP/DOWN. Compared with the FLAT group, participants in the UP group had a significantly higher likelihood of achieving ≥3% weight loss (adjusted odds ratio 2.45, 95% CI 1.78-3.38). Long-term tracking of step counts using the Asmile app revealed distinct activity patterns. Continuous increases in step counts were associated with the greatest likelihood of weight loss, emphasizing the importance of sustained physical activity. These findings support the use of long-term step monitoring to guide interventions for obesity and lifestyle-related disease prevention.
Deciphering the directionality of information flow in cortical circuits is essential for understanding brain dynamics, learning, and neuroplasticity after injury. However, current noninvasive methods cannot distinguish bottom-up from top-down signals across entire networks, including deep brain regions. Here, we present UltraFast Layer-Resolved Encoding (uFLARE) that combines ultrafast-fMRI with a Layer-based Connective Field (lCF) model to disentangle bottom-up from top-down signaling. Our findings reveal that lCF size, an indicator of information integration, differentiates bottom-up and top-down activity through distinct layer-specific connectivity patterns during spontaneous activity, challenging the previous suggestions that bottom-up signals are solely stimulus-driven. Bottom-up connectivity follows an inverted U-shape, peaking in layer IV, while top-down exhibits a U-shaped pattern, with peaks in layers I and VI. These profiles generalize across sensory pathways (visual, somatosensory, and motor) and reveal injury-induced network reorganization, such as LGN bypassing V1 to provide direct bottom-up input to higher visual areas.
Ultraviolet (UV) radiation is a major factor contributing to skin aging. Ferroptosis, a recently identified form of regulated cell death, remains controversial in its role in mid‑wave ultraviolet (UVB)‑induced skin photoaging. Preliminary evidence suggests that Dual‑Specificity Phosphatase 1 (DUSP1) may be associated with both skin photoaging and ferroptosis. This study aims to investigate the role of ferroptosis and the regulatory mechanism of DUSP1 in a UVB‑induced stress‑induced premature senescence (UVB‑SIPS) model of human dermal fibroblasts (HDFs). Our findings demonstrate that ferroptosis occurs in HDFs following UVB irradiation. Treatment with a low concentration (0.5 µM) of the ferroptosis inhibitor ferrostatin‑1 (Fer‑1) alleviated UVB‑induced senescence, reduced intracellular reactive oxygen species (ROS) accumulation, and promoted the expression of type I and type III collagen. We also observed a decrease in DUSP1 protein expression in HDFs after UVB exposure. Furthermore, in vitro knockdown of DUSP1 exacerbated cellular senescence, impaired proliferative capacity, intensified cell‑cycle arrest, upregulated the expression of senescence‑associated proteins (p53, p21, p16), and reduced the production of type I and type III collagen. Subsequent experiments indicated that DUSP1 knockdown may promote ferroptosis by down‑regulating the SLC7A11/GPX4 axis, thereby accelerating UVB‑induced photoaging in HDFs. These results suggest that DUSP1 might serve as a novel therapeutic target for mitigating skin photoaging.
The felting of wool directly on the sheep largely affects its value as a raw material for the textile industry. In this regard, the aim of this study was to investigate the amino acid and mineral composition of wool affected by this defect in sheep of the Ukrainian Carpathian Mountain breed. Experimental wool samples were divided into guard and down fibers. The amino acid composition was determined using an AAA-400 amino acid analyzer, the mineral composition was determined using an atomic absorption spectrophotometer (Thermo Scientific iCE 3500), and sulfur was determined by the nephelometric method based on the turbidity of a barium sulfate suspension stabilized with glycerin. It has been shown that the process of wool felting is accompanied by partial degradation of fibers resulting from the destruction of disulfide, ionic, and hydrogen bonds, as indicated by a significant decrease in the total amino acid content, due to reductions in aspartic (P < 0.01) and glutamic (P < 0.01) acids, arginine (P < 0.05), as well as cystine (P < 0.01) and histidine (P < 0.05) in down fibers, and lysine (P < 0.01) in guard fibers. The observed decrease in calcium and copper content in felted wool indicates a disruption of ionic interactions with the functional groups of amino acids, which play a key role in stabilizing the structural organization of wool fibers, while the decrease in sulfur content in down fibers confirms the destruction of disulfide bonds. Therefore, the results of the study indicate that wool felting is the result of biochemical processes leading to disruption of the keratin structure of the fiber. In the future, the obtained data may be used to develop comprehensive approaches aimed at preventing and eliminating this wool defect.
SARS-CoV-2 spike protein is continuously evolving, leading to new variants. While mutations in the receptor-binding domain (RBD) enhance binding to the ACE2 receptor and evade neutralizing antibodies, the function of mutations in the N-terminal domain (NTD) remains poorly understood. Using two independent methods, surface plasmon resonance (SPR) and cryo-EM, we show that NTD mutations increase the population of spike protein with the RBD in the "up" conformational state. SPR association and dissociation kinetics of spike binding to ACE2 and antibodies, analyzed using a coupled equilibrium model, determined the relative populations and indicated that the RBD-up-to-down transition is rate-limiting relative to the RBD-down-to-up transition. Advanced model fitting of cryo-EM Coulomb potential maps confirmed the populations. The combined effect of NTD and RBD mutations exceeds the sum of their individual effects, indicating long-range allosteric communication and energetic coupling within the spike protein.
Z-DNA Binding Protein 1 (ZBP1) is a critical pattern recognition receptor within the innate immune response to viral infection. ZBP1 senses foreign nucleic acids in the unusual, left-handed Z-conformation via binding through its N-terminal Zα1 and Zα2 domains and activates downstream pro-pyroptotic, -apoptotic, and -necroptotic pathways to initiate cell death and allow for viral clearance. Both dsDNA and dsRNA can adopt the Z-conformation, however, the conformational change is energetically expensive, especially for dsRNA, and typically requires chemical modifications or protein binding to induce a right-to-left-handed conversion and stabilization. ZBP1 has been previously shown to bind and convert B-DNA to the Z-conformation and was assumed to be able to convert A-RNA as well, despite the lack of experimental validation. Here, we use a variety of Nuclear Magnetic Resonance (NMR) and other biophysical and biochemical experiments to characterize the Z-DNA and Z-RNA binding properties of ZBP1's Zα1 and Zα2 domains. While ZBP1's Zα domains are able to convert and stabilize unmodified dsDNA in the Z-conformation, both domains are incapable of flipping unmodified A-conformation dsRNA. We show that ZBP1's Zα domains require dsRNAs with Z-promoting chemical modification in order for them to bind and stabilize the Z-conformation. These results contrast with the Zα domain from Adenosine Deaminase Acting on RNA 1 (ADAR1), which can bind and flip both dsDNA and dsRNA into the Z-conformation, potentially indicating finely tuned competition between ADAR1 and ZBP1 for pro-survival and pro-death outcomes, respectively. This work highlights the functional variability of Zα domains and narrows down the potential physiological substrates of ZBP1 in infection and disease.
Information theory has inspired numerous advancements in multi-view learning. Most multi-view methods incorporating information-theoretic principles rely an assumption called multi-view redundancy which states that common information between views is necessary and sufficient for down-stream tasks. This assumption emphasizes the importance of common information for prediction, but inherently ignores the potential of unique information in each view that could be predictive to the task. In this paper, we propose a comprehensive information-theoretic multi-view learning framework named CIML, which discards the assumption of multi-view redundancy. Specifically, CIML considers the potential predictive capabilities of both common and unique information based on information theory. First, the common representation learning maximizes G´acs-K¨orner common information to extract shared features and then compresses this information to learn task-relevant representations based on the Information Bottleneck (IB). For unique representation learning, IB is employed to achieve the most compressed unique representation for each view while simultaneously minimizing the mutual information between unique and common representations, as well as among different unique representations. Importantly, we theoretically prove that the learned joint representation is predictively sufficient for the downstream task. Extensive experimental results have demonstrated the superiority of our model over several state-of-art methods. The code is released on CIML.
Information processing in the cortex depends on the integration of bottom-up and top-down signals through recurrent microcircuits spanning layers. Although the canonical microcircuit provides a framework for this integration, how these interactions are implemented at synapse resolution remains unclear. Here, we use large-volume electron microscopy reconstructions of mouse primary visual cortex to map the intralaminar and interlaminar connectivity of intratelencephalic (IT) neurons in layers 2/3 and 5. We find that layer 2/3 IT neurons formed a depth-dependent gradient of recurrent connectivity, with superficial (L2) and deeper (L3) neurons potentially forming two channels associated with bottom-up and top-down processing, respectively. These channels are preserved across layers via cell-type-specific pathways involving distinct L5 IT types, rather than collapsing into a single integrative pool. Moreover, each channel is regulated by a largely separate cohort of inhibitory interneurons, stabilizing recurrent excitation while limiting crosstalk. Together, these results reveal parallel, cell-type-specific processing streams embedded within the canonical circuit.
Dam-calf contact (DCC) rearing is a form of cow-calf contact (CCC) in which dairy cows nurse their calves for some months until weaning while additionally being milked throughout lactation. Growing implementation, consumer demands, and research interest indicate that CCC and DCC are viable systems for the dairy industry. However, machine milking in these systems presents notable challenges with multifactorial drivers. Those are discussed in this review based on current scientific knowledge regarding milking in nursing dams: Machine milk yield (MMY), flow and fat content of the harvested milk are reduced compared to non-nursing controls while protein and lactose levels vary and udder health is unaffected or improved. In systems with full-time DCC, relative MMY reduction can reach 60-70% during the nursing period whereas highly restrictive suckling regimes cause smaller MMY losses but may not meet the calf's nutritional needs. Post-weaning and lactation MMY can be reduced or unaffected. Low udder fills at the start of milking delay milk let-down potentially conflicting with standardized milking procedures and machine settings. A 0.5-1.5% decline in milk fat concentration indicates incomplete milk ejection and incomplete udder emptying which can further reduce MMY. These effects likely reflect a disturbance of the milk ejection reflex, as in nursing dams, suckling is a more potential stimulus for oxytocin (OT) release than milking. Underlying central mechanisms of inhibited OT release at milking in nursing dams may be related to the cow-calf bond affecting the dams' oxytocinergic system but the complexity of required experimental set-ups compromises research in cattle. In bonded dams, multisensory stimulation by the calf may be a stronger trigger for OT release than the milking procedure. Further, separation from the calf during milking and dam-individual variation regarding the ability to release milk in response to machine stimulation may play a role. Zooming out, social scientific studies reveal that DCC farmers see poor milkability as an unsolved challenge. However, it is not limited to nursing dams, as stress affects milk ejection. To quantify incomplete udder emptying, research should refine strip milk fat analysis for on-farm use. Cow-individual milk ejection dynamics must be better understood to assess if breeding for better milk let-down in response to machine milking while maintaining good maternity traits can improve milkability in DCC systems.
This investigation reports the effects of Lactiplantibacillus plantarum CQPC03 (LP-CQPC03) on preventing thrombus formation and reducing intestinal oxidative stress and inflammation in a carrageenan-induced mouse thrombosis model. High-throughput 16S rRNA sequencing determined the composition of intestinal microorganisms. Biochemical reagents, section observations, and quantitative polymerase chain reaction (qPCR) identified mouse serum and tissue-related markers. Experimental findings show that LP-CQPC03 enhances activated partial thromboplastin time (APTT) and decreases thrombin time (TT), fibrinogen (FIB), and prothrombin time (PT). LP-CQPC03 also significantly reduces black tail severity in thrombotic mice. Moreover, LP-CQPC03 lowers malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), nuclear factor kappa-B (NF-κB), and interleukin-1 beta (IL-1β) levels in thrombotic mouse serum, while increasing superoxide dismutase (SOD) and catalase (CAT) activities. Hematoxylin and eosin (H&E) pathological analysis reveals that LP-CQPC03 lessens tissue damage caused by tail vein thrombosis. In the colon tissues of thrombotic mice, LP-CQPC03 up-regulates the mRNA expression of copper/zinc superoxide dismutase (Cu/Zn-SOD), manganese superoxide dismutase (Mn-SOD), and CAT, while down-regulating NF-κB p65, IL-6, TNF-α, and interferon gamma (IFN-γ). In tail vein vascular tissues, LP-CQPC03 also suppresses the mRNA expression of NF-κB p65, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Gut microbiota sequencing results show that LP-CQPC03 increases the population of beneficial bacteria and decreases harmful ones. These findings demonstrate that LP-CQPC03 prevents thrombosis in mice, reduces oxidative stress and intestinal inflammation, and regulates gut microbiota by increasing beneficial bacteria. A high concentration of LP-CQPC03 shows a better effect, comparable to heparin.