Cisplatin is a widely used chemotherapeutic agent for triple-negative breast cancer (TNBC), but resistance remains a major challenge. Understanding the molecular alterations driving this resistance is essential for identifying therapeutic targets. In this study, we employed an integrated proteomics and lipidomics approach to elucidate key pathways associated with cisplatin resistance. Employing high-resolution mass spectrometry, we conducted a comparative analysis between cisplatin-resistant (cisR) and cisplatin-sensitive (cisS) TNBC cell lines to discover resistance-associated alterations in protein and lipid expression. Proteomic analysis revealed overexpression of extracellular matrix (ECM) remodeling proteins, COL6A1, COL6A2, COL6A3, and VTN, that support epithelial-mesenchymal transition (EMT) and chemoresistance. Membrane-associated proteins such as TIMP2, MMP14, and APP were also elevated, indicating enhanced invasive and pro-survival signaling. Lipidomic alterations, including upregulation of FABP3, FABP4, LPL, and downregulation of PLA2G4A, indicated increased lipid uptake, metabolic rewiring, and membrane restructuring. Notably, elevated long-chain phosphatidylcholines and decreased sphingomyelins suggested increased membrane rigidity and reduced cisplatin permeability. Additionally, dysregulation of CDK activity through CCND2, CCND3, and CCNB2 overexpression indicated accelerated cell cycle progression and evasion of DNA damage checkpoints. Together, this integrative analysis highlights ECM remodeling, cytoskeletal dynamics, and lipid metabolism as major contributors to cisplatin resistance and identifies potential therapeutic markers for TNBC.

The global rise of antimicrobial resistance (AMR) in Enterobacterales, including the Enterobacter cloacae complex, is narrowing treatment options. Tigecycline, a last-resort antibiotic for the treatment of multidrug-resistant (MDR) Gram-negative pathogens, is increasingly compromised by emerging resistance mechanisms, notably efflux pump overexpression and regulatory network adaptation. In this study, sixty clinical isolates of Enterobacter cloacae (thirty-eight tigecycline-resistant [TGC-R], twenty-two tigecycline-susceptible [TGC-S]) were analyzed to investigate gene expression changes in efflux pumps and regulatory genes under tigecycline pressure (1/2 minimum inhibitory concentration [MIC]) and standard conditions. Tigecycline exposure markedly increased tolC and acrA together with the regulators marA and ramA, while acrB increased only modestly. This indicates a strong regulatory component to the tigecycline response. In contrast, TGC-S isolates exhibited significant induction of marA, marB without corresponding activation of efflux pumps. Δlog2FC analysis highlighted distinct transcriptional shifts between exposed and unexposed groups, with resistant strains displaying greater divergence. Heatmaps and boxplot visualizations, supported by Wilcoxon test statistics, underscored the regulatory responses associated with tigecycline pressure. These findings indicate that, alongside AcrAB-TolC upregulation, stress-responsive regulators (marA, ramA) are strongly induced by sub-inhibitory tigecycline, underscoring the multifactorial regulation of tigecycline response in the E. cloacae complex.

This study investigated the impact of α-amino adipic semialdehyde (AAS)-mediated lysine carbonylation on the thermal gelation of porcine myosin. Purified myosin (2 mg/mL) was pre-treated with N-Ethylmaleimide to block the sulfhydryl groups, then oxidized in a metal-catalyzed oxidation system (10 μM FeCl₃, 100 μM ascorbic acid, and 5 mM H₂O₂) with varying l-lysine concentrations (0-60 mM) for 24 h at 4 °C. Physiochemical attributes, structural conformation, and rheological properties (G') of myosin were systematically monitored. Following heat-induced gelation (20-80 °C), the resulting gels were evaluated for water-holding capacity (WHC), microstructure, and intermolecular forces. Results showed that oxidation significantly induced myosin carboxylation, evidenced by a substantial increase in both total carbonyl and AAS contents. This oxidative stress triggered a decrease in protein solubility, increased turbidity and particle size, and the disruption of α-helix and tertiary structures. Consequently, the WHC and G' of the resulting gel declined markedly, characterized by a more porous and disordered microstructural network. Conversely, the addition of l-lysine effectively attenuated AAS formation in a dose-dependent manner, thereby mitigating the oxidative impairment of myosin's physiochemical and structural properties and preserving its gelation functionalities. These results indicate that AAS-mediated lysine carbonylation plays a detrimental role in myosin structural integrity and gelation performance. Furthermore, the incorporation of exogenous l-lysine offers a potential strategy to mitigate oxidative deterioration in muscle protein systems.

The application of yeast protein (YP) in food industry is often limited by its undesirable flavor. While the Maillard reaction (MR) enhances protein flavor effectively, excessive glycation can also promote the development of advanced glycation end products (AGEs). This study elucidated the mechanism by which oligomeric proanthocyanidins (OPCs) inhibit AGE formation in glycated YP (GYP) and synergistically enhance flavor. The results showed that OPC synergistic MR reduced the content of bitter flavor in YP, changed the distribution of volatile compounds, and decreased the content of bitter amino acids. Furthermore, OPC binding dose-dependently reduced the formation of early, intermediate, and AGEs in GYP. Structural analysis revealed that OPC binding modified the secondary and tertiary structures of YP, which effectively reduced protein carbonylation, protected thiol groups, and inhibited protein aggregation, thereby contributing to the improved flavor. The anti-glycation activity of OPC was achieved by scavenging reactive free radicals (O₂-· and OH·), chelating metal ions (Fe2+), and trapping of α-Dicarbonyl compounds. Moreover, OPC has a stronger affinity for YP than glucose (Glu), and it inhibited the glycation process by competing with Glu for the occupation of glycation sites. These findings provide critical insights for developing OPC as natural anti-glycation agents to improve the flavor and safety of protein-based foods.

Lentinan, a β-glucan extracted from Lentinus edodes, has been reported to exert potent antitumor activity. However, its underlying mechanism in breast cancer (BRCA) remains insufficiently elucidated. In this study, we investigated the direct antitumor effects of the water-extracted Lentinus edodes polysaccharide (WLNT) on human BRCA both in vitro and in vivo. Upon intravenous administration, WLNT reached the tumor site, peaked at 30 min and remained detectable for up to 2 h. Treatment with 1 mg/mL WLNT markedly suppressed tumor growth. Specifically, WLNT inhibits BRCA growth by downregulating the expression of CD133, a key marker of breast cancer stem cells. In addition, proteomic screening revealed that WLNT significantly downregulated the expression of SCGB2A2 (mammaglobin-A), whose levels are associated with the CD133 concentration in cells. Notably, SCGB2A2 was identified to promote BRCA cell proliferation, migration and xenograft tumor growth. We identified a novel anti-BRCA mechanism of WLNT in downregulating SCGB2A2 expression. Further investigation revealed that CD133 directly interacted with SCGB2A2 and accelerated its lysosomal degradation in cells under physiological conditions. WLNT competitively binds to CD133, inhibiting its interaction with SCGB2A2. In summary, our study demonstrates the critical role of the tumor-promoting effectors CD133 and SCGB2A2 in the anti-BRCA activity of WLNT, providing a new perspective for the study of the antitumor mechanism of lentinan.

Circadian rhythms are endogenous regulatory mechanisms evolved by organisms to adapt to periodic light-dark changes. Circadian rhythms can regulate the pathogenicity of fungal pathogens, but the underlying mechanisms remain unclear. Casein kinase 2 (CK2) is an essential component for the normal functioning of fungal circadian rhythms, with the CKa gene encoding its alpha subunit. To investigate the action mechanism of JGM in the pathogenicity of the rice blast fungus via circadian rhythm, ΔMocka and ΔMocka' mutants was generated using gene-editing technology. We observed that the deletion of Mocka resulted in altered amplitudes and phases of circadian rhythm genes relative to the wild type (WT). Additionally, the Mocka deletion influenced the sporulation capacity of Magnaporthe oryzae as well as infectivity. Jinggangmycin (JGM) is an aminoglycoside antibiotic primarily used to control rice sheath blight. The use of JGM has been shown to increase the antioxidant capacity of rice seedlings by enhancing the activity of catalase (CAT) and peroxidase (POD), and it causes the differential expression of rice resistance genes. The deletion of the Mocka gene in M. oryzae weakened its ability to suppress the rice immune response and led to a reduced antioxidant capacity and a significant decrease in callose deposition in rice. Also, the effect of JGM on wild-type M. oryzae was associated with the circadian rhythm. We suggest that Mocka plays a critical role in the pathogenicity of M. oryzae and its circadian rhythm, and the circadian rhythm of the fungus has an impact on the inhibitory effect exerted by JGM. In summary, our findings deepen our understanding of the interconnections between JGM and the rice blast fungus's pathogenicity as well as the pathogenic mechanisms involving circadian rhythm. This research provides a theoretical basis and potential targets for both photoperiod-coordinated precise pesticide application strategies and the development of novel fungicides.

In Northern Europe, climate warming is driving the northward expansion of deciduous tree species such as aspen and silver birch, while simultaneously intensifying biotic stress from pests and pathogens. This creates an urgent need for improved understanding of molecular defence mechanisms underlying stress resistance and resilience in temperate forest trees, as a basis for the development of innovative biotechnological approaches. However, progress in this area remains limited by the lack of reproducible experimental systems and well-characterized molecular markers for systemic defence responses in deciduous tree species. In this study, we aimed to identify and validate known plant defence gene markers associated with systemic stress responses in hybrid aspen and silver birch to support future functional research. Using sequence mining and phylogenetic analyses, we identified homologues of biotic stress-response genes in the genomes of both species. We then employed in vitro propagated tree clones to assess defence gene activation in distal leaves following systemic signal induction by leaf wounding and bacterial flagellin treatment at 4 and 24 hours post-induction. We identified LOX2, MPK3, and EIN2 as early wounding-responsive genes in silver birch, while JAZ10 together with EIN2 showed robust induction in hybrid aspen in response to the combined effects of wounding and flagellin. Collectively, these findings establish a reproducible in vitro framework for validating stress responsive genes and provide a foundation for future studies of systemic signalling, tree-microbe interactions, and stress resilience in ecologically and economically important forest tree species.

The dysregulation of N6-methyladenosine (m6A) modification drives progression in non-small cell lung cancer (NSCLC), yet its interplay with traditional medicine-derived therapeutics remains largely unexplored. We propose a novel strategy that integrates m6A-based prognostic subtypes with Pueraria pharmacology to identify prognostic markers and therapeutic targets related to m6A regulators for NSCLC treatment. Multi-omics clustering of 1,661 NSCLC samples identified three distinct m6A modification patterns. Based on these, a robust 19-gene prognostic signature was constructed via Cox regression and validated in the GSE31210 dataset. This risk model significantly correlated with immune infiltration and patient survival. Furthermore, the expression patterns of these genes were validated via single-cell RNA-sequencing (scRNA-seq) and RT-qPCR in NSCLC cell lines. To identify pharmacological interventions, we intersected the m6A prognostic signature with 7,333 NSCLC-related genes and 366 Pueraria targets, revealing IGFBP1 as the core therapeutic nexus. Immunohistochemistry confirmed the expression of IGFBP1 in NSCLC tissues. Molecular docking and 100-ns molecular dynamics (MD) simulations confirmed stable binding of Pueraria compounds to IGFBP1, specifically 7,8,4'-trihydroxyisoflavone (binding energy = -8.3 kcal/mol) and genistein (-7.4 kcal/mol). This study establishes IGFBP1 as a therapeutic nexus connecting m6A-driven NSCLC progression and the anti-tumor effects of Pueraria. Our RNA-modification-guided pharmacology approach advances the integration of traditional medicines into precision oncology.

Entinostat, a selective HDAC1/3 inhibitor, has shown anti-tumor activity in small cell lung cancer (SCLC), but the precise molecular mechanisms underlying its efficacy remain incompletely understood. This study aimed to investigate the functional role and mechanism of Entinostat in SCLC, with a focus on HDAC1 inhibition and its downstream effects on cell death pathways. The anti-tumor effects of Entinostat were evaluated in SCLC cell lines and a xenograft mouse model using MTT, flow cytometry, immunofluorescence, western blotting, and rescue experiments with HDAC1 overexpression and pathway-specific inhibitors. We found that Entinostat significantly inhibited SCLC cell viability and induced both apoptosis and autophagy. Mechanistically, Entinostat downregulated HDAC1 protein levels, increased p53 acetylation and phosphorylation, activated AMPK, and suppressed mTOR signaling. HDAC1 overexpression reversed these molecular changes and attenuated Entinostat-induced cytotoxicity. In vivo, Entinostat suppressed tumor growth and consistently modulated the HDAC1/p53/AMPK/mTOR pathway. In conclusion, Entinostat exerts potent anti-tumor activity in SCLC by simultaneously inducing apoptosis and autophagy through epigenetic modulation of p53 via HDAC1 inhibition and subsequent regulation of the AMPK/mTOR axis.

Salt stress severely impacts a plant's root development. This study explores the role of volatile organic compounds (VOCs) from Trichoderma harzianum ST02 in enhancing adventitious root development of peppermint (Mentha × piperita), an important salt-tolerant medicinal plant, under salt stress. Peppermint seedlings were subjected to NaCl concentrations (0, 50, 100, and 150 mM) with or without exposure to T. harzianum ST02 VOCs. Morphological analyses revealed that VOCs significantly increased adventitious root numbers and total root length under salt stress, alleviating NaCl-induced damage. Gas chromatography-mass spectrometry (GC-MS) analysis found 3(2H)-furanone, dihydro-2-methyl, as a predominant component in T. harzianum ST02 VOCs. Transcriptomic analysis via RNA sequencing (RNA-seq) for four groups under different treatments identified 5589 differentially expressed genes (DEGs), with 298 DEGs specifically linked to VOCs exposure under 100 mM NaCl stress. Functional annotation indicated enrichment in pathways related to secondary metabolism and plant hormone signal transduction. VOCs modulated key genes, including those encoding ion transporters (e.g., SLAH2 and ABCG14), reactive oxygen species (ROS) scavenging (e.g., peroxidases), and cell wall-modifying enzymes (e.g., XTH). Notably, VOCs downregulated genes involved in abscisic acid (ABA) and ethylene biosynthesis (NCED3, ACS, and ACO), reducing stress signaling, while upregulating auxin (GH3.1) and gibberellin (GA2ox) metabolism genes, promoting root development. These findings suggest that T. harzianum ST02 VOCs enhance peppermint's salt tolerance by coordinately regulating hormone signaling, ion transport, and cell wall remodeling, thereby facilitating adventitious root development. Our work provides a molecular framework for utilizing beneficial microbes to improve plant resilience in saline environments.

Using the whole-genome data of Atractylodes lancea, members of the auxin(Aux)/indole-3-acetic acid(IAA) gene family were identified and characterized, and the effects of 1-naphthaleneacetic acid(NAA) treatment on the expression levels of this gene family were investigated, providing a foundation for further studies on the functions of the A. lancea Aux(AlAux)/IAA gene family. Members of the AlAux/IAA gene family were identified from the A. lancea whole-genome data using TBtools-Ⅱ. Bioinformatics software was employed to analyze the physicochemical properties of the encoded proteins, construct a phylogenetic tree, and predict conserved motifs and gene structures. Tissue-cultured seedlings of A. lancea were used as experimental materials, and key genes of the AlAux/IAA gene family were screened by transcriptome sequencing. The expression of key AlAux/IAA genes was analyzed after one month of NAA treatment. A total of 53 AlAux/IAA genes were identified from the A. lancea genome. Most AlAux/IAA proteins were localized in the nucleus, lacked transmembrane domains, and exhibited negative hydrophobicity. Among them, 44 AlAux/IAA genes were predicted to encode functional Aux/IAA transport proteins. Transcriptome sequencing and RT-qPCR analyses showed that the AlAux/IAA family genes exhibited spatiotemporal expression specificity, and different members displayed varying response times and intensities to NAA treatment. Tissue-specific expression analysis revealed that the AlAux/IAA gene family was generally highly expressed in flowers. This study identified the Aux/IAA gene family members in A. lancea, preliminarily analyzed their sequence characteristics, and examined their expression features in response to Aux. It is speculated that AlAux/IAA13 and AlAux/IAA38 may be involved in rooting and bud growth and development during the subculture process of A. lancea tissue-cultured seedlings. These results provide a theoretical basis for elucidating the molecular mechanisms of AlAux/IAA gene function and Aux-mediated regulation of rhizome growth in A. lancea.

Carbapenem-resistant Acinetobacter baumannii (CRAB) has appeared as a leading cause of hospital-acquired infections, resulting in high mortality rates and limited treatment options. The development of novel antibacterial agents has lagged behind the rapid spread of antibiotic-resistant bacteria; thus, alternative therapeutic strategies are urgently needed. In this study, we investigated plumbagin, a natural compound derived from Plumbago zeylanica L., for its potential antibacterial and antibiofilm activities against CRAB. MIC and MBC determinations showed that plumbagin significantly inhibited growth and exerted bactericidal activity at low concentrations. Biofilm inhibition concentration and biofilm eradication concentration assays revealed that plumbagin both prevented biofilm formation and eradicated mature biofilms. Consistent with these findings, XTT reduction assays showed a marked decrease in metabolic activity after plumbagin treatment, and confocal laser scanning microscopy with COMSTAT analysis confirmed reduced biofilm biomass and decreased viability of biofilm-embedded cells. Further, quantitative polymerase chain reaction confirmed the downregulation of the carbapenem-resistance gene blaOXA-23 and biofilm-related genes, including bfmR, csuA/B, ompA, and bap. Collectively, these results reveal plumbagin as a therapeutic candidate against CRAB.

Multiple myeloma (MM) is an incurable tumor of malignant plasma cells. Importin α4, also known as KPNA3, is a component of the importin α/β system, which contributes to the cytosol-to-nucleus trafficking of cellular substances. In this study, we discovered that KPNA3 was highly expressed in MM and that its expression level inversely correlated with patient prognosis. Both in vitro and in vivo experiments demonstrated that the knockdown of KPNA3 inhibited the proliferation of MM cells, promoted their apoptosis and increased their drug sensitivity. Mechanistic investigations also revealed that the knockdown of KPNA3 inhibited ALDH2 transcription and downregulated the activity of the hedgehog pathway. Additionally, we demonstrated the direct binding of ivermectin (IVM) to KPNA3, a functional component of the importin α/β system. IVM can significantly reduce KPNA3 protein levels and promote apoptosis in MM cells. Finally, both in vitro and in vivo experiments revealed that IVM and selinexor exhibited synergistic anti-MM activities. Overall, our study reveals the role of KPNA3 in MM and suggests that targeting its nuclear import is a promising MM treatment.

Despite advances in therapeutic regimens for managing cancer progression, ovarian cancer (OVC) still depends on platinum-based chemotherapy as its first-line treatment. Acquired resistance is accompanied by abnormal alterations in epigenetic regulation; however, in-depth mechanistic studies on cisplatin-resistant OVC are lacking. Herein, we show that abnormal overexpression of histone lysine demethylase 5B (KDM5B), but not KDM5A, strongly correlates with cisplatin resistance and OVC tumor progression. Genome-wide sequencing data revealed that KDM5B removes H3K4me3 from the promoter of dual-specificity phosphatase 4 (DUSP4), activating the MAPK pathway to increase cisplatin resistance. We also found that KDM5B protein stability is dynamically controlled via the ubiquitin-proteasome system (UPS), which is mediated by ubiquitin-specific protease 7 (USP7), F-box and WD repeat domain-containing 7 (FBXW7), and homeodomain-interacting protein kinase 1 (HIPK1). KDM5B and USP7 depletion effectively resensitizes OVC to cisplatin resistance, whereas DUSP4 silencing results in resistance in vitro and in vivo. Targeting KDM5B and USP7 synergistically represses tumor progression and increases sensitivity to cisplatin. Overall, we propose two new UPS-associated proteins, USP7 and FBXW7, which are responsible for abnormal KDM5B protein regulation, and suggest a novel mechanism to overcome cisplatin resistance in OVC by targeting the KDM5B-DUSP4 axis.

Multiple myeloma (MM) is characterized by kidney deficiency, phlegm, and blood stasis as core findings, specifically in Traditional Chinese Medicine (TCM), and the kidney-tonifying, phlegm-resolving, and blood stasis-removing (KPR) method is a fundamental therapeutic approach for MM in TCM. Western medicine primarily focuses on targeted immunotherapy or chemotherapy for MM treatment, whereas TCM characterizes MM through distinct pathological patterns that directly correspond to immune microenvironment dysregulation. Emerging evidence implicates the PHD finger protein 19 (PHF19)/enhancer of zeste homolog 2 (EZH2)/trimethylated histone H3 at lysine 27 (H3K27me3) epigenetic axis in immune microenvironment dysregulation and MM progression. Notably, TCM "blood stasis" correlates with hypoxia-induced immune gene silencing in MM bone marrow, and KPR (a clinically validated TCM decoction with 16 herbs) acts on this axis via its active components that regulate EZH2 and epigenetic function, merging TCM syndrome differentiation with modern epigenetics. We have designed a randomized controlled trial (RCT) to investigate the mechanism of action and safety of the KPR method in MM.

Pyriproxyfen (PPF) and diflubenzuron (DFB) are widely used pesticides with metabolic toxicity in humans underexplored. White adipose tissue (WAT) is a potential target for endocrine-disrupting chemicals.

Esophageal adenocarcinoma (EAC) is an aggressive malignancy with poor patient outcomes and limited therapeutic options. WEE1, a G2/M checkpoint kinase, is often upregulated in cancers and associated with resistance to therapy. In this study, we identify a previously unrecognized cytoplasmic role of WEE1 in stabilizing the oncogenic transcription factor MYC and promoting drug resistance in EAC. WEE1 was found to be aberrantly overexpressed and mislocalized to the cytoplasm in EAC cell lines and patient samples. WEE1 depletion or inhibition by MK-1775 significantly reduced MYC protein levels and transcriptional activity by promoting proteasome-mediated degradation. Mechanistically, WEE1 inhibition activated GSK3β, leading to phosphorylation of MYC at threonine 58 and subsequent ubiquitin-dependent degradation. In contrast, overexpression of wild-type WEE1, but not a kinase-dead mutant (K328A), increased p-CDC2 (Y15) and MYC protein levels, confirming that WEE1's kinase activity is essential for maintaining MYC stability. WEE1 inhibition also downregulated the MYC-ABCC1 axis, decreased MRP1 expression, and impaired drug efflux. A high-throughput screen of 892 FDA-approved compounds identified the histone deacetylase inhibitor Panobinostat as a potent synergistic partner of MK-1775. Combination treatment induced robust apoptosis and markedly suppressed tumor growth in EAC organoids and patient-derived xenograft models. These findings reveal a novel cytoplasmic function of WEE1 in sustaining MYC stability and chemoresistance. Targeting WEE1 destabilizes MYC and enhances therapeutic response, supporting the combination of MK-1775 and Panobinostat as a promising treatment strategy for EAC.

Aristolochic acid (AA), commonly used in Chinese herbal medicine to treat various diseases, can cause acute kidney injury (AKI). The pregnane X receptor (PXR), a nuclear receptor, is involved in drug metabolism, carcinogenesis, inflammation, apoptosis, oxidative stress and energy metabolism. Here, we demonstrate that PXR plays a protective role in AA-induced AKI. First, PXR expression was dramatically decreased in mice and Boston University mouse proximal tubular (BUMPT) cells treated with AA. Overexpression of PXR in BUMPT cells alleviated apoptosis induced by AA in vitro. The specific agonist of PXR pregnenolone carbonitrile (PCN) relieved AA-induced AKI in mice, while the PXR inhibitor ketoconazole exacerbated the damage caused by AA in mice. Mechanistically, PXR bound to p53 in BUMPT cells and led to the ubiquitination and degradation of p53, thereby downregulating its expression. Taken as a whole, our data demonstrate that PXR may protect against AA-induced AKI by suppressing p53 expression.

Fibroblasts are crucial in tissue engineering because of their ability to synthesize the extracellular matrix (ECM) and secrete growth factors. Orbital fibroblasts (OFs) from patients with thyroid eye disease (TED) exhibit enhanced fibroblastic properties, making them ideal candidates for regenerative medicine in ocular tissue. In the present study, we investigated the effect of nanoperlite on TED OFs. Nanoperlite, with its unique properties including high silica (SiO2) content, holds promise for enhancing fibroblast functions. Nanoperlite was prepared and characterized in terms of particle size and chemical composition. A sample of orbital adipose tissue was taken from a TED patient during orbital decompression surgery and OFs were expanded in vitro. The cells were then treated with nanoperlite at concentrations of 1 and 10 μg/mL for 24 h, and gene expression related to the fibrogenesis process was assessed using real-time PCR. Nanoperlite at 1 μg/mL significantly increased the expression of TGF-β, CD90, α-SMA, ZEB1, β-Catenin, and Snail genes in OFs. However, at 10 μg/mL, this effect was not observed. This study highlights nanoperlite's potential to enhance fibroblast activity specifically at the concentration of 1 μg/mL. This effect can potentially aid tissue engineering strategy for periorbital tissue repair and eyelid reconstruction. However, further research is needed to fully elucidate its therapeutic potential and safety profile.

Alcoholic liver disease (ALD) is driven by oxidative stress, lipid metabolism, inflammation, and apoptosis. Current therapies lack efficacy in targeting multi-pathway mechanisms. Xing-Pi-Qing-Gan decoction (XPQG) is an improved traditional Chinese medicine designed to alleviate ALD, but its molecular mechanism remains unknown.