Cardiovascular diseases (CVDs) remain a leading cause of global morbidity and mortality. Their complex and multifactorial pathogenesis, involving endothelial dysfunction, chronic inflammation, oxidative stress, metabolic dysregulation, and pathological remodeling, limits the long-term effectiveness of current therapeutic strategies and underscores the need for novel treatment approaches. Plant-derived extracellular vesicles (PDEVs) have recently emerged as promising cardioprotective agents because of their favorable biocompatibility, relatively low immunogenicity, abundant endogenous bioactive cargoes, and engineering flexibility. Owing to these properties, PDEVs possess dual characteristics as natural nanocarriers and bioactive therapeutic agents. Preclinical evidence from various in vitro and in vivo cardiovascular disease models indicates that PDEVs exert antioxidative, anti-inflammatory, immunomodulatory, and tissue-reparative effects, thereby attenuating myocardial injury, reducing oxidative stress, and promoting cardiomyocyte survival. Beyond their intrinsic therapeutic activities, PDEVs can also serve as multifunctional drug delivery vehicles for small-molecule drugs, nucleic acids, proteins, and natural bioactive compounds, improving cargo stability, bioavailability, and therapeutic performance. Recent advances in surface functionalization, membrane fusion, and biomimetic design have further enhanced their targeting capacity and functional controllability. This review focuses on the application of PDEVs in cardiovascular disease therapy, systematically summarizing their preparation, characterization, quality evaluation, and relative advantages and limitations compared with conventional nanocarriers. It further highlights their therapeutic effects in different cardiovascular disease models, drug delivery applications, engineering strategies, and the current progress and key challenges in clinical translation. Continued advances in this field may promote the translation of PDEVs from experimental research to clinical application and broaden their value in cardiovascular nanomedicine. λ PDEVs exhibit excellent biocompatibility and minimal immunogenicity, making them ideal for cardiovascular applications. λ Advanced techniques for PDEVs isolation and characterization enable stringent quality control and reproducibility. λ PDEVs protect the heart through antioxidant, anti-inflammatory, anti-apoptotic, and reparative effects in various cardiovascular diseases. λ PDEVs as therapeutic agents and engineered PDEVs for drug delivery promote clinical application and translational potential.

This study was conducted to explore the mechanism of Sea Buckthorn Granules (SBG) in treating chronic bronchitis (CB) in rats. The primary chemical components of SBG were identified using UPLC-Q-TOF-MS/MS. A rat model of CB was established through smoke inhalation combined with lipopolysaccharide (LPS) stimulation, followed by oral administration of SBG. The serum levels of TNF-α, IL-6, and IL-1β in rats were measured using ELISA. Pathological changes in lung tissues were observed through HE and toluidine blue staining. Furthermore, the main components and pathways involved in the therapeutic effects of SBG on CB were predicted using network pharmacology. In addition, p38 and NF-κBp65 protein expression as well as their phosphorylation levels in rat lung tissues were measured by western blot. Compared to the model group, treatment with SBG significantly alleviated cough symptoms, and Mitigating body weight loss in CB rats (P<0.05). SBG markedly decreased serum levels of TNF-α, IL-6, and IL-1β (P<0.05); as well as reduction in both NF-κBp65 expression levels and p38 phosphorylation within lung tissues (P<0.05). In summary, SBG can effectively ameliorate cough symptoms while reducing serum TNF-α, IL-6, and IL-1β levels, as well as inhibiting the MAPK/NF-κB signaling pathway.

Background: Osteoarthritis (OA) is a prevalent, chronic joint disease. Jintiange capsules (JTG), approved by the State Food and Drug Administration of China for orthopedic diseases, have shown noticeable benefits in treating chronic conditions through traditional Chinese medicine. Synovial mesenchymal stem cell-derived exosomes (SMSC-Exos) can modulate articular chondrocytes (ACs), but how pharmacological agents alter miRNA content in SMSC-Exos and influence ACs remains unclear. Methods: OA was induced in rats using type II collagenase, followed by a 30-day JTG regimen. Therapeutic efficacy was assessed by weight-bearing and mechanical allodynia tests, micro-CT, and Safranin-Fast Green staining. Differential miRNAs after JTG treatment were profiled by transcriptome analysis. JTG constituents were characterized via UPLC-Q-TOF-MS, and core targets/pathways were predicted by network pharmacology. Exosomes from JTG-treated SMSCs (SMSC-JTG-Exos) were tested in vitro on ACs to evaluate cell activity, migration, apoptosis, and key pathway gene/protein expression. Results: JTG ameliorated OA phenotypes in vivo. Transcriptomics identified nine miRNAs differentially expressed after JTG treatment. Integrating chemical profiling with network pharmacology highlighted ten core genes and implicated the rheumatoid arthritis signaling pathway, centering on miRNA-214-3p regulation. In vitro, SMSC-JTG-Exos enhanced ACs activity and migration, reduced apoptosis, and down-regulated related protein expression. Conclusion: JTG alleviates OA, at least in part, by up-regulating miRNA-214-3p in SMSC-Exos, which enhances ACs viability and suppresses apoptosis. The underlying mechanism likely involves modulation of the rheumatoid arthritis signaling pathway, suggesting an exosome-miRNAmediated route by which JTG exerts chondroprotective effects.

Tremella fuciformis polysaccharides (TFPs), as one of the pivotal functional constituents of T. fuciformis, have attracted increasing attention because of their diverse health-promoting activities. At present, TFPs have garnered considerable interest from researchers worldwide owing to their broad spectrum of biological effects, including antitumor, anti-inflammatory, immunomodulatory, gut-regulatory, anti-obesity, antidiabetic, hepatoprotective, radioprotective, antioxidant, neuroprotective, and anti-aging activities. However, the development and utilization of TFP-based functional foods and therapeutic products have been substantially constrained by the limited understanding of their structure-activity relationships (SARs), potential applications, and safety profiles. In this review, we provide a comprehensive overview of the extraction, purification, structural characteristics, pharmacological properties, and underlying mechanisms of TFPs. In addition, the structure-activity relationships, potential applications, safety evaluation, and modification strategies associated with their bioactivities are highlighted, together with a discussion of future research directions. This review is intended to provide a theoretical basis for the further investigation and application of TFPs in cosmetics, functional foods, beverages, and healthcare products.

INTRODUCTION:This study aimed to investigate the protective effects of Siji Kangbingdu Mixture (SKM) against acute lung injury (ALI) in mice and to elucidate its underlying mechanisms. METHODS:ALI was induced in Kunming mice via intranasal administration of LPS (5 mg/kg), followed by oral SKM treatment for 7 days. Lung wet-to-dry (W/D) ratio, histopathology, multiomics analysis, and network pharmacology were performed. Key targets and pathways were identified through dynamic KEGG analysis and validated by Western blotting. RESULTS:SKM treatment ameliorated alveolar hemorrhage, alveolar wall disruption, septal thickening, edema, and inflammatory cell infiltration. Integrated multi-omics analysis revealed that SKM primarily modulated the Ras signaling pathway, reducing the protein expression of Phospho- MEK1/2, Raf1, Phospho-ERK1/2, and RASH/RASK/RASN, thereby contributing to the treatment of ALI. DISCUSSION:SKM alleviated LPS-induced ALI in mice by inhibiting the Ras pathway, highlighting the pathway's role in ALI pathogenesis. However, due to limitations of the animal model and incomplete validation, further studies combining clinical research and in vitro experiments are needed to confirm its efficacy and mechanism. CONCLUSIONS:SKM shows potential to ameliorate ALI by suppressing inflammatory responses and reducing local tissue fibrosis. The combination of metabolomics, transcriptomics, and network pharmacology elucidated its mechanism, while Western blot analysis suggested that its therapeutic effect is associated with downregulation of the Ras signaling pathway.

Purpose:Knee osteoarthritis (KOA) is a chronic degenerative joint disease and recognized as the fourth leading cause of disability worldwide. Despite the proven clinical efficacy of electroacupuncture (EA) in alleviating KOA-related symptoms, the precise molecular mechanisms underlying its therapeutic effects remain incompletely elucidated. The purpose of this study is to determine and validate the potential therapeutic targets and mechanism of EA for KOA through a combined approach of in vivo experiments and transcriptomics analysis. Methods:A total of 40 SD rats were randomly divided into four groups: control group, model group, two-course EA intervention group, and four-course EA treatment group. The KOA model was established with monosodium iodoacetate (MIA) intra-articular injection. The EA treatment groups received intervention at the Yanglingquan and Dubi acupoints. The control group received no intervention. All four groups underwent behavioral assessments (rat knee joint diameter and bilateral foot balance test), joint pathological analysis (Micro-CT and hematoxylin and eosin staining) to evaluate the effect of EA on KOA. Transcriptomics, GO analysis and KEGG analysis were applied to predict potential targets. Potential targets were further verified via Western blot (WB). Results:EA could significantly reduce knee joint diameters and improve the supporting force of KOA rats. Micro-CT revealed that EA increased the subchondral bone mass of KOA rats. ELISA results suggest that the levels of interleukin-1β and tumor necrosis factor-α decreased after EA intervention. The transcriptomics analysis revealed that EA could downregulate the levels of phospho (p)-p38 mitogen-activated protein kinase (MAPK), p-extracellular signal-regulated kinase (ERK), and p-cAMP response element-binding protein (CREB) which is further verified via WB. Conclusion:EA intervention significantly ameliorated KOA-induced degeneration of cartilage and subchondral bone, improved pain-associated behavioral performance, alleviated inflammation. The molecular mechanism is related to the inhibition of the p-p38 MAPK/ERK/CREB pathway.

BACKGROUND:Intestinal fibrosis is a common complication of Crohn's disease, for which effective therapies remain lacking. Wumei Wan (WMW), a classical traditional Chinese medicine formula, has been used for nearly two millennia to treat inflammatory bowel disease and its complications. PURPOSE:This study aimed to evaluate the antifibrotic effects of WMW and to elucidate its underlying mechanisms. METHODS:The therapeutic effects of WMW were evaluated in a dextran sulfate sodium-induced mouse model of intestinal fibrosis and further validated in a colitis-associated colorectal cancer model. Multi-omics sequencing and bioinformatics analyses were used to elucidate the pharmacological mechanisms of WMW, and complementary experiments were performed to verify the roles of butyrate and butyrate-associated bacteria. RESULTS:WMW exhibited significant antifibrotic efficacy in mouse models. Further analysis revealed that WMW alleviated fibrosis by remodeling the gut microbiota and promoting endogenous butyrate production, thereby suppressing FAK-Src-mediated mechanotransduction, preventing Yes-associated protein nuclear translocation, and inhibiting colonic fibroblast activation. In microbiota-depleted mice, the inhibitory effects of WMW on butyrate production and mechanotransduction were markedly diminished. Notably, supplementation with Bacteroides fragilis produced antifibrotic effects concordant with those of WMW and butyrate and effectively reduced intestinal fibrosis. CONCLUSION:This study demonstrates that WMW alleviates intestinal fibrosis by targeting the microbiota-metabolite-mechanotransduction axis. WMW and butyrate-associated bacteria may therefore represent promising antifibrotic strategies.

Ulcerative colitis (UC) is a chronic inflammatory colon disease that is a major public health problem. The long-term administration of traditional drugs is likely to trigger adverse reactions. The myrrh essential oil (MEO) exhibits promising therapeutic efficacy against ulcerative colitis. However, due to the inherent instability and volatility of MEO, it was formulated into myrrh essential oil microemulsion (MM) with the aim of enhancing its stability. This study explored the optimal formulation for synthesizing MM, and a series of relevant indices were employed to meticulously investigate its stability characteristics. In animal experiments, a UC mouse model was established with the assistance of Dextran Sulfate Sodium (DSS). The therapeutic efficacy was comprehensively evaluated by recording Disease Activity Index (DAI) scores, detecting the levels of Tumor Necrosis Factor-α (TNF-α) and Interleukin-1β (IL-1β), and observing the morphological features of mouse colonic tissues through hematoxylin-eosin (HE) staining and immunohistochemistry (IHC) techniques. The results confirmed that both MEO and MM are effective in treating ulcerative colitis.

Background: Cervicitis is a common gynecological disease, which triggers local inflammation and tissue damage by a complex mechanism, seriously affecting women's health. Chinese medicine plays a prominent role in the treatment of gynecological inflammation. Shuangshi Tongling Capsule (SSTL), as a traditional Chinese medicine (TCM) compound, needs to be further elucidated for the treatment of cervicitis. Methods: Cervicitis was induced with 25% phenol gel (except controls), followed by 12-day intragastric treatment. Outcomes included genital inflammation scores, uterine index, and histopathology (HE staining). Serum tumor necrosis factor-alpha (TNF-alpha), Interleukin(IL)-6, IL-8, and IL-1[3 were measured via ELISA. Integrated metabolomics-transcriptomics and Western blotting identified mechanistic pathways. Results: SSTL alleviated cervicitis in rats by improving uterine histopathology, reducing external genital inflammation scores (P < 0.01 vs. model), and reversing uterine hypertrophy (P < 0.05). Serum pro-inflammatory cytokines (TNF-alpha, IL-1[3, IL-6, IL-8) were suppressed (P < 0.01), with concurrent weight restoration. Multi-omics analysis identified AMPK signaling as pivotal, validated by downregulation of p-NF-kappa B (P < 0.05) and upregulation of p-AMPK/SIRT1 (P < 0.05) in uterine tissues, indicating SSTL mitigates inflammation through AMPK/NF-kappa B/SIRT1 modulation. Conclusion: This study found that SSTL ameliorates cervicitis in rats through the expression of AMPK pathway-related proteins.

Background:Colon cancer ranks as the third most common malignant tumor globally. Due to incomplete surgical resection and the multidrug resistance of tumor cells, it exhibits a high postoperative recurrence rate. Consequently, there is an urgent need to develop novel therapeutic strategies to inhibit postoperative recurrence of colon cancer. Methods:Thermosensitive liposomes (Bu&Ap-Lip) co-loaded with bufalin (Bu) and apatinib (Ap) were prepared via the thin-film hydration method, with optimization of Prescription Processes. Bu&Ap-Lip was co-encapsulated with new indocyanine green (IR820) within an injectable PLGA-PEG-PLGA hydrogel, establishing a photothermally responsive composite hydrogel (Bu&Ap-Lip@IR820 Gel). The system characterized the physicochemical properties, rheological characteristics, and drug release behavior of the hydrogel, and further evaluated its in vitro antitumor activity and in vivo efficacy against postoperative recurrence of colon cancer. Results:Bu&Ap-Lip@IR820 Gel demonstrated excellent injectability and photothermally responsive drug-release properties. In vitro cellular experiments demonstrated that Bu&Ap-Lip@IR820 Gel effectively inhibited tumor cell migration, invasion, and angiogenesis. In vivo studies revealed that this liposome hydrogel prolonged local drug retention. When combined with near-infrared light irradiation, Bu&Ap-Lip@IR820 Gel significantly suppressed tumor recurrence while exhibiting favorable in vivo biocompatibility. Conclusion:This study developed a NIR-responsive composite liposome hydrogel integrating Bu multi-targeted antitumor properties, Ap anti-angiogenic effects, and IR820 photothermal therapeutic advantages. Through near-infrared responsiveness, it achieves localized precision drug release, effectively suppressing postoperative recurrence. This provides a novel and promising strategy for the clinical prevention and treatment of colon cancer recurrence.

ETHNOPHARMACOLOGICAL RELEVANCE:Xinxue Granules (XXGR) is a traditional Chinese medicine formula derived from the classical prescription Zixue Powder, one of the three treasured formulas in traditional Chinese medicine. Based on the principle of heat-clearing and detoxification, it has long been used to treat respiratory diseases associated with heat-toxin accumulation. Owing to its multi-component nature, XXGR has been reported to modulate inflammatory responses and alleviate pulmonary injury. However, its protective effects and underlying mechanisms in pulmonary fibrosis-like injury remain unclear. AIM OF THE STUDY:To investigate the protective effects and mechanisms of XXGR in pulmonary fibrosis. A bleomycin-induced pulmonary fibrosis-like injury mice model was established after random grouping. The therapeutic effects were assessed by histopathological and biochemical analyses. Network pharmacology, metabolomics, and transcriptomics were integrated to identify potential pathways. Additional in vitro experiments using TGF-β1-induced MLE-12 cells, including EPAC inhibition with ESI-09, were performed to further explore the underlying mechanism. MATERIALS AND METHODS:A bleomycin (BLM)-induced pulmonary fibrosis (PF) mouse model was established to evaluate the antifibrotic effects of XXGR. Ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) was used to characterize the chemical constituents and serum-absorbed components of XXGR. Network pharmacology, transcriptomics, and non-targeted metabolomics were integrated to identify potential targets and pathways. In vivo experiments, including histopathology, biochemical assays, quantitative real-time PCR (qRT-PCR), and Western blotting (WB), were performed to validate key molecular mechanisms. In vitro experiments using TGF-β1-stimulated MLE-12 cells with EPAC inhibition (ESI-09) were performed to explore mechanisms. Molecular docking was conducted to evaluate compound-target interactions. All botanical names were verified according to the World Flora Online. RESULTS:UPLC-Q-TOF/MS identified 20 blood-absorbed components of XXGR, and network pharmacology revealed 222 potential targets, highlighting the cyclic adenosine monophosphate (cAMP) signaling pathway. XXGR reduced lung injury, inflammatory cytokine levels, fibroblast activation, and extracellular matrix deposition in BLM-induced mice. Mechanistically, XXGR increased EPAC expression and CREB phosphorylation while decreasing GLI3 expression in vivo and in vitro, consistent with activation of cAMP signaling. EPAC inhibition with ESI-09 partially reversed the effects of XXGR on fibrosis- and EMT-related markers. CONCLUSION:XXGR attenuated bleomycin-induced pulmonary fibrosis-like injury by suppressing inflammation and fibroblast activation. Its protective effects may be partially mediated via the cAMP/EPAC/CREB signaling pathway. These findings suggest that XXGR represents a promising multi-target therapeutic candidate for pulmonary fibrosis.

ABSTRACT Cardiovascular inflammation is increasingly recognized not merely as a secondary response to hemodynamic or metabolic injury, but as a determinant of disease initiation, progression, and remodeling. In the injured heart and vasculature, danger sensing, inflammatory priming, inflammasome activation, nucleic acid recognition, immunometabolic rewiring, immunothrombosis, adaptive immune remodeling, and defective resolution form interdependent circuits rather than isolated pathways. A key challenge is to understand how these circuits shift from adaptive clearance and repair to persistent immune activation, fibrosis, and functional decline. Here, we synthesize evidence on immune landscapes and core inflammatory networks in cardiovascular diseases, focusing on TLR–NF‐κB signaling, NLRP3 inflammasomes, cGAS–STING‐dependent cytosolic DNA sensing, alternative mitochondrial nucleic acid‐sensing platforms, and redox‐immunometabolic gating. We highlight mitochondrial quality control and mitochondria‐derived DAMPs, including mtDNA, mtROS, ATP, cardiolipin, and oxidized lipids, as an upstream interface linking metabolic stress to sterile immune activation. We further organize disease‐specific inflammatory patterns through a stage‐cell‐threshold perspective across ischemic injury, vascular and metabolic disease, and cardiomyopathic remodeling. Finally, we discuss network‐guided therapeutic strategies, translational limitations, biomarkers, endpoints, and safety considerations. This integrated perspective provides a conceptual basis for moving cardiovascular inflammatory therapy from broad suppression toward more precise network regulation.

Glycyrrhizic acid (GL) and glycyrrhetinic acid (GA) exhibit antitumor activity, favorable biocompatibility, receptor-targeting capabilities, and amphiphilicity. These properties make them promising multifunctional components for developing antitumor drug delivery systems. Unlike previous reviews that focus on individual applications, this review systematically categorizes GL/GA according to their three functional roles. First, as therapeutic agents, GL/GA can be incorporated into passively targeted, actively targeted, and stimuli-responsive nanocarriers. They can be combined with chemotherapeutic drugs, such as cisplatin and paclitaxel, to enhance therapeutic efficacy and reduce systemic toxicity. Second, as targeting ligands, GL/GA can be conjugated to the surfaces of nanocarriers to enable receptor-mediated tumor delivery. Finally, as self-assembling materials, GL/GA can co-assemble with other drugs to form carrier-free nanostructures. Alternatively, they can serve as building blocks for polymeric carriers. These strategies enable drug-carrier integration, simplify formulation processes, and enhance synergistic antitumor effects. Furthermore, this review analyzes the key challenges in the clinical translation of these formulations. These challenges include the complexity of large-scale production, insufficient in vivo stability, a lack of long-term safety data, and inconsistencies in quality evaluation systems. Future translational prospects are also outlined to guide the rational design and clinical development of natural product-based nanomedicines.

Background: Disorders of metabolism can affect the food intake, weight changes, and behavioral alterations of the body. Metabolic disorders are usually accompanied by the occurrence of diseases. We aimed to study the effects of the compatibility of Paeoniae Radix Rubra (PRR) and Angelicae Sinensis Radix (ASR) on the metabolic level of rats, and observe the changes in body weight and behavior. Discover the mechanism of preventing the occurrence of diseases by using PRR and ASR. Methods: Two animal models were induced by levothyroxine and low-temperature stimulation, followed by 21 days of edible traditional Chinese medicine administration. The changes in the rats' water intake, food intake, body temperature, and thermotactic behavior were recorded. Results: The results showed that PRR could cause an increase in the body weight of rats, a decrease in body temperature, and a stronger preference for warm environments. PRR inhibited thyroid function, the excitability of the nervous system, and energy metabolism. PRR upregulated the expressions of mTOR and TRPM8 while downregulating the expressions of AMPK and TRPV1. Conclusion: Our research findings suggest that the cold-natured PRR can inhibit the material and energy metabolism of the body and lower the body temperature, increasing the thermophilic behavior of rats. In contrast, ASR exhibited an antagonistic effect against PRR.

Chinese herbal medicine-derived extracellular vesicles (CHM-EVs) have recently emerged as promising naturally derived nanocarriers for drug delivery. These nanoscale membranous vesicles inherit diverse bioactive constituents from their parental medicinal plants, including lipids, proteins, nucleic acids, and small-molecule metabolites, thereby endowing them with both intrinsic bioactivity and delivery capability. Owing to their lipid bilayer structure, CHM-EVs can encapsulate or associate with both hydrophilic and hydrophobic cargos, improving drug stability, solubility, and bioavailability while potentially reducing systemic toxicity and enhancing target-site accumulation. In parallel, engineering strategies such as surface functionalization, lipid reconstitution, membrane coating, and biomimetic synthesis have further expanded their potential for targeted delivery, controlled release, and scalable production. This review systematically summarizes the biogenesis, sources, compositional features, isolation and purification strategies, and physicochemical characterization of CHM-EVs. Recent advances in cargo-loading approaches and their applications in the delivery of chemical drugs, nucleic acids, and proteins are also comprehensively discussed. In addition, the key advantages of CHM-EVs as biomimetic delivery platforms, together with the major barriers to their clinical translation, are critically evaluated. Overall, this review provides a comprehensive overview of CHM-EVs and may facilitate both the modernization of traditional Chinese medicine and the development of next-generation drug delivery systems based on naturally derived vesicular platforms.

To elucidate sediment formation in Baihe Gujin oral liquid (BGO) and optimize its stabilization, this study used ultrahigh-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS), physicochemical analysis, surfactant screening, zeta potential measurement, and high-performance liquid chromatography (HPLC) fingerprinting. The precipitate mainly contained hydrophobic constituents (organic acids, flavonoids, alkaloids) with low flexibility and high logP. Surfactant screening showed that Tween 80 most effectively stabilized the system, reducing turbidity from 202.5 ± 1.0 to 118.0 ± 0.2 NTU, particle size from 5334.7 ± 2178.5 to 587.5 ± 36.3 nm, and PDI from 1.000 ± 0.000 to 0.495 ± 0.074, while increasing absolute zeta potential from -10.8 ± 1.3 to -28.6 ± 1.7 mV. Concentration optimization identified 0.6% Tween 80 as optimal, achieving turbidity of 110.6 ± 0.5 NTU, particle size of 321.9 ± 103.0 nm, PDI of 0.299 ± 0.034, and zeta potential of -32.4 ± 1.8 mV. Higher concentrations (0.7%-0.8%) reduced performance. HPLC fingerprints showed no major chemical changes after Tween 80 addition (similarity > 0.9). Thus, 0.6% Tween 80 improves BGO stability via micellar solubilization and electrostatic repulsion without altering the material basis.

Rheumatoid arthritis (RA) is an autoimmune disorder marked by chronic synovitis and systemic complications. The Gentiana macrophylla-Angelica pubescens (Qinjiao-Duhuo, Q-D) pair offers anti-RA potential but suffers from low oral bioavailability. Transdermal delivery bypasses gastrointestinal irritation and first-pass effects, but stratum corneum barriers limit permeability. Natural penetration enhancers, Zanthoxylum bungeanum essential oil (ZBEO) enhances drug penetration and alleviates inflammation in RA models, suggesting synergistic benefits with Q-D extracts. However, the mechanism is not fully understood. The purpose of this study was to investigate the transdermal permeation mechanism of ZBEO on Q-D and its synergistic anti-RA effect. A total of 533 compounds were analyzed from UPLC-Q-Exactive Orbitrap MS of Q-D. Seven core components of Q-D for the therapy of RA were identified, and the PI3K-AKT signaling pathway was identified as the primary action pathway. As demonstrated by ATR-FTIR and other techniques, ZBEO increased the cumulative transmission of key components of Q-D. This was achieved by disrupting the lipid arrangement of the skin stratum corneum, among other processes. The cellular assay demonstrated that ZBEO-Q-D significantly inhibited the proliferation of MH7A cells and lowered the levels of inflammatory factors. In vivo investigations revealed that ZBEO-Q-D significantly alleviated the symptoms of RA rats. In this study, ZBEO enhanced the transdermal penetration efficiency of the key components of Q-D by enhancing the lipid mobility of the stratum corneum and enlarging the cell gap and alleviated the synovial inflammation of RA, which provided a new strategy for the treatment of RA with Chinese herbal medicine administered transdermally.

Ethnopharmacological relevance Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality worldwide, placing a substantial economic burden on both individuals and societies. In recent years, traditional Chinese medicine (TCM) has attracted increasing attention for its advantages in treating CVD, owing to its efficacy and relatively few side effects. Among various TCM formulations, Wenxin Keli (WXKL) has demonstrated promising therapeutic efficacy in the treatment of CVD. Aim of the review This paper presents a comprehensive summary of the chemical composition, quality control, pharmacological activities, safety profile and clinical applications of WXKL, derived from extensive literature searches in major electronic databases. Furthermore, the current challenges facing WXKL and future perspectives for future research are discussed. Materials and methods A comprehensive literature search was performed in the following electronic databases up to 2025: PubMed, Web of Science, Google Scholar, China National Knowledge Infrastructure, and WANFANG Data. The review process was conducted in accordance with the PRISMA guidelines. Results Previous studies indicate that WXKL is effective in treating patients with CVD and is associated with comparatively fewer adverse reactions. This review aims to elucidate the relationship between the anti-CVD effects of WXKL and mechanisms involving oxidative stress, inflammation, myocardial ion channels and other factors, while also summarizing current evidence regarding its safety profile. Conclusions WXKL exerts therapeutic effects in CVD treatment through multiple mechanisms including anti-inflammatory and anti-oxidant stress, modulation of myocardial ion channel homeostasis, inhibition of apoptosis, and prevention of myocardial ischemia, cardiac fibrosis and cardiac hypertrophy. However, additional clinical trials and animal studies are still required to further substantiate its efficacy and guide clinical application. This review summarizes current research on WXKL and aims to provide insights to inform future investigations.

Pickering emulsions (PEs) stabilized by solid particles have gained increasing interest in food systems as alternatives to surfactant-based emulsions, owing to their superior physical stability, reduced toxicity, and compatibility with clean-label formulations. However, many food-grade particles exhibit limited interfacial activity, sensitivity to environmental conditions, or insufficient robustness during processing, while existing reviews often provide descriptive summaries rather than mechanistic integration across particle properties and functional performance. This review examines food-grade PEs from an interfacial engineering perspective, systematically analyzing how intrinsic particle characteristics and advanced particle design strategies regulate emulsion formation, stability, and functionality. Modification approaches are evaluated with respect to their interfacial mechanisms, food compatibility. Bibliometric analysis is further employed to identify research evolution, emerging trends, and application hotspots in food and related systems. This work provides a critical, mechanism-oriented framework that bridges fundamental interfacial science with application-driven formulation, offering guidance for the rational design of next-generation food-grade PEs.

Eczema, a chronic inflammatory skin condition, causes persistent discomfort and impairs patients' quality of life. Cnidium monnieri has been traditionally used for its anti-inflammatory and antipruritic properties. The present study aimed to develop an optimized formulation of Cnidium monnieri volatile oil cream (CMVOC) and evaluate its anti-inflammatory effects in an eczema model. A single-factor and response surface optimization approach was used to determine the optimal cream formulation. The formulation was evaluated based on appearance, physical stability, particle size and moisturizing capacity. An eczema model was induced using 2,4-dinitrochlorobenzene (DNCB) in mice. Serum levels of IL-6 and IL-17 were measured by ELISA, skin pathology was assessed by hematoxylin and eosin and toluidine blue staining and JAK2/STAT3 expression was detected by immunohistochemistry to determine the activation status of the related signaling pathway. The optimized formulation contained 4.45 g octadecanol, 4 g Vaseline, 2.2 g liquid paraffin, 0.81 g isopropyl myristate Estergel®, 1.6 g Cnidium monnieri volatile oil, 0.39 g sodium dodecyl sulfate, 1.16 g glycerol, 0.04 g nibergin ethyl ester and 25.35 g Distilled Water. In vivo, CMVOC markedly improved skin lesions in DNCB-induced mice, reduced serum IL-6 and IL-17 levels and alleviated epidermal thickening, edema and inflammatory infiltration. Immunohistochemistry further demonstrated suppressed activation of the JAK2-STAT3 signaling pathway. CMVOC effectively mitigated eczema-related inflammation by reducing pro-inflammatory cytokines and inhibiting JAK2-STAT3 pathway activation, providing experimental support for its potential as a topical therapy for eczema.