Fibrosis is characterized by excessive extracellular matrix (ECM) deposition driven by sustained pro-fibrotic signaling and underlies a wide range of pathological conditions. Accordingly, strategies that broadly suppress ECM production are considered promising for the treatment of fibrosis. Although calcium hydroxyapatite (CaHA) is primarily used as a nanoparticle-based dermal filler, previous observations that it affects collagen production suggest its potential repurposing as a regulator of ECM-related programs. Here, we investigated the anti-fibrotic efficacy of CaHA and the signaling mechanisms underlying its effects. CaHA broadly suppressed ECM-related gene expression in fibroblasts, extending beyond collagen to multiple ECM components and associated regulatory factors. Mechanistically, CaHA attenuated Piezo1-associated Ca2+ signaling and was also associated with activation of the PKA pathway. Importantly, CaHA similarly reduced ECM-related gene expression in a fibrotic liver cell model, supporting the broader relevance of its anti-fibrotic activity. Together, these findings identify CaHA as a broad suppressor of ECM-related gene expression through modulation of Piezo1-associated Ca2+ signaling and PKA-associated pathways, and support its potential as an anti-fibrotic therapeutic strategy.
Pandalus hypsinotus (P. hypsinotus), also known as coonstripe shrimp, has high economic value and is widely distributed in Alaska, the Bering Sea and the East Sea of Korea. However, owing to the low catch rates and patchy spatial distribution, transcriptome-based studies on this species remain limited. Transcriptome analyses using PacBio Iso-Seq and Illumina RNA sequencing techniques were performed to establish a de novo unigene set of P. hypsinotus and identify differentially expressed genes (DEGs) in the hepatopancreas compared to the tail muscle. A search of all the unigenes against Gene Ontology (GO), KEGG, Pfam, BLASTN, and UniProt resulted in 46,703 annotated unigenes. A comparison of the sequences in the two tissue-derived libraries revealed 9,429 DEGs in the hepatopancreas. We also investigated the small RNAomes of P. hypsinotus using the Illumina small RNA sequencing technology. Because miRNAs are highly sensitive to stress responses and pathogen infections, they serve as effective indicators of the immune status, thereby acting as crucial tools for enhancing productivity and disease control in the aquaculture industry. The 130 identified microRNA (miRNA) candidates were classified into 32 orthologous and 98 novel miRNAs using BLASTN and miRBase. Through GO analysis and direct interactions between miRNAs and genes, the differentially expressed miRNAs (DEMs) and DEGs related to immune responses showed regulatory relationships based on their sequences. These findings provide a valuable resource for future studies on novel gene detection, gene mapping and biological pathways that may be regulated by miRNAs unique to P. hypsinotus.
Spermatogonial stem cells (SSCs) are responsible for lifelong spermatogenesis in adult males; however, their scarcity and inherent heterogeneity, coupled with the lack of robust SSC-specific surface markers, continue to impede isolation and characterization. In the present study, we found CD71, which corresponds to transferrin receptor (TfR1; encoded by Tfrc), a candidate marker capable of enriching for SSC populations from mouse testes. The immunohistochemistry detected co-localization of CD71 with the undifferentiated spermatogonia marker glial cell line-derived neurotrophic factor family receptor alpha 1 (GFRα1) on the seminiferous basement membrane, with approximately 81% co-localization. Consistent with this finding, the expression of Tfrc was up-regulated in SSC-enriched germ cell populations relative to mouse germ cell lines (GC-1 and GC-2) and somatic cell lines from testis (TM3 and TM4). Fluorescence-activated cell sorting (FACS) analysis further showed that GFRα1+ cells exhibited approximately 1.4-fold higher Tfrc mRNA expression than GFRα1- cells. Similarly, CD71+ cells exhibited significantly higher expression of the undifferentiated spermatogonia markers Id4, Lhx1, Gfrα1, Zbtb16, and Etv5. Functional transplantation assays further demonstrate that CD71high cells give rise to approximately 5.5-fold more colonies than freshy isolated, FACS-unsorted donor cells. Moreover, peanut agglutinin (PNA) lectin staining confirmed the normal spermatogenic differentiation within colonies derived from CD71high donor cells. Our findings collectively indicate that CD71high cells represent an SSC-enriched population with enhanced spermatogenic regenerative capacity and support the use of CD71 as a complementary marker for SSC enrichment and fertility restoration.
Hepatic inflammation plays a key role in acute and chronic liver diseases by driving hepatocellular injury and promoting disease progression. However, the molecular mechanisms that maintain hepatic immune homeostasis remain unclear. Cathepsin A (Ctsa), a lysosomal serine carboxypeptidase involved in protein degradation and enzyme stabilization, has been implicated in lysosomal storage disorders. However, its role in liver immunity is poorly understood. Given the emerging evidence that lysosomal proteases contribute to immune regulation and inflammatory signaling, Ctsa is a promising yet underexplored candidate for elucidating how lysosomal proteases influence hepatic inflammation. To address this gap, this study aimed to investigate Ctsa function using Ctsa knockout (Ctsa-/-) mice. Under basal conditions, Ctsa-/- mice exhibited splenic immune activation and relative hepatomegaly accompanied by histological alterations. Following lipopolysaccharide challenge, the mice developed aggravated liver injury with elevated aminotransferase levels, enhanced immune cell infiltration, and increased pro-inflammatory cytokine expression. These inflammatory changes were accompanied by increased hepatocellular apoptosis, as evidenced by elevated Bax/Bcl-2 ratio, cleaved caspase-3 expression, and increased TUNEL-positive cells. Collectively, these findings indicate that Ctsa contributes to the regulation of hepatic immune and cellular homeostasis, and its loss increases susceptibility to inflammatory liver injury.
Derivation of electrophysiologically mature cardiomyocytes from human pluripotent stem cells (hPSCs) remains a prerequisite for effective cardiac modeling and preclinical drug evaluation. However, current differentiation protocols often produce heterogeneous cell populations with limited maturity. In this study, we developed a CD47-based fluorescence-activated cell sorting strategy to purify ventricular-like cardiomyocytes from three-dimensionally differentiated hPSC-derived spheroids. CD47+ cardiomyocytes exhibited highly consistent contractile behavior and enhanced structural maturation, as confirmed using immunocytochemistry for myosin regulatory light chain 2 ventricular/cardiac muscle isoform and α-actinin. Electrophysiological analysis using a patch clamp revealed that the majority of CD47+ cells displayed ventricular-like action potential waveforms, characterized by prolonged repolarization duration, elevated amplitude, and a reduced negative maximum diastolic potential. Drug responsiveness was assessed using multi-electrode array recordings. CD47-enriched cardiomyocytes demonstrated reproducible and dose-dependent field potential alterations in response to known cardiotoxic agents, including remdesivir and quinidine, and outperformed metabolically purified controls in sensitivity and inter-replicate consistency analysis. These results establish CD47 as a reliable surface marker for isolating mature ventricular-like cardiomyocytes from hPSCs. The method enables the generation of functionally robust cardiomyocyte populations suitable for in vitro cardiac research and pharmacological testing.
Social isolation and inadequate group composition can severely impair brood survival in eusocial insects due to the loss of social interactions. Establishing small artificial colonies is a prerequisite for studying developmental biology and functional genetics in ants; however, the minimal social requirements for effective brood rearing remain poorly understood. In this study, we investigated the impact of social composition - specifically the presence of pupae and worker abundance - on the survival and development of intact eggs within laboratory-maintained sub-colonies of the pharaoh ant, Monomorium pharaonis. Our analysis revealed that supplementing colonies with pupae significantly enhanced brood survival and accelerated larval development. Furthermore, we identified that sufficient worker numbers improve brood success, supporting the existence of a viable colony size. Our data suggest that while a sufficient workforce is essential for brood care, further increases in worker number do not yield proportional gains in rearing efficiency under our laboratory conditions. These results indicate that establishing favorable rearing conditions depends on achieving a functional demographic balance, particularly through pupal supplementation and an appropriate worker ratio. This study highlights the vital role of colony demographics and pupal presence in ant development, providing a practical framework for brood manipulation and ensuring baseline survival for future functional genetic applications.
Many individuals who initially present with depression later develop manic or hypomanic episodes, yet the biological processes accompanying this delayed shift remain unclear. Here, we examined whether perturbation of the adult hippocampal neurogenic niche is associated with time-dependent shifts in mood-relevant behaviors. Using Nestin-CreER::Rosa26-FloxedSTOP-DTa (Nestin-DTa) mice, we induced partial ablation of Nestin-positive adult neural stem cells (aNSCs) in the hippocampus by tamoxifen administration and assessed phenotypes at 4 and 8 weeks post-ablation. Neurogenic-lineage populations in the dentate gyrus were quantified by immunohistochemistry using stage-specific markers. Partial aNSC ablation reduced the Nestin-positive pool and BrdU-labeled proliferation, followed by a compensatory expansion of proliferative progenitors and DCX-positive neuroblasts. At 4 weeks, Nestin-DTa mice exhibited anxiety-like behavior and increased forced-swim immobility. By 8 weeks, anxiety-like measures normalized, and mice displayed increased exploratory/locomotor activity and reduced forced-swim immobility, accompanied by sustained elevation of progenitor and immature neuronal compartments. These findings provide a tractable model in which disruption of the adult neurogenic niche is associated with a transition from depression-like behavior to a hyperactive, mania-like phenotype over time.
Oral lichen planus (OLP) is a chronic, immune-mediated inflammatory disease of the oral mucosa that can cause persistent pain and has a recognized, though relatively low, risk of malignant transformation. Recent studies have identified oxidative and nitrosative stress as key contributors to the pathophysiology of OLP. Excessive production of reactive oxygen and nitrogen species, combined with reduced antioxidant defenses, leads to cellular damage, including lipid peroxidation, protein modification, and DNA injury. This oxidative imbalance drives keratinocyte apoptosis and sustains inflammatory signaling, creating a pro-inflammatory tissue environment. In parallel, metabolic dysfunction is increasingly recognized in OLP, characterized by altered energy production and nutrient utilization that disrupt tissue homeostasis. These two processes are closely linked, as oxidative stress impairs metabolic pathways, while metabolic alterations further increase oxidative burden, forming a self-reinforcing cycle that perpetuates mucosal injury and chronic inflammation. Clinically, markers of oxidative stress and metabolic imbalance, particularly those detectable in saliva, show promise for non-invasive diagnosis and risk assessment. Therapeutic strategies aimed at restoring redox balance and improving metabolic regulation represent emerging avenues beyond conventional symptom management. Understanding the crosstalk between oxidative stress and metabolism offers new opportunities for precision medicine approaches to improve the diagnosis, treatment, and long-term outcomes of patients with OLP.
TAR DNA-binding protein 43 (TDP-43) is a DNA- and RNA-binding protein that regulates gene expression by modulating transcription and RNA processing. It plays pivotal roles in neuronal development and function, and its mislocalization and aggregation are major pathological features of several neurodegenerative diseases. However, the regulatory mechanisms that control Tdp-43 expression and activity during the transition from embryonic stem cells (ESCs) to neural progenitor cells (NPCs) remain poorly understood. Through integrative epigenomic and transcriptomic analyses, we identified multiple intergenic and intragenic enhancers within and around the Tdp-43 locus that generate enhancer RNAs (eRNAs). These eRNAs exhibit dynamic, region-specific expression changes and modulate Tdp-43 transcription in a stage- and context-dependent manner. Specifically, a subset of eRNAs was highly expressed in ESCs and downregulated upon differentiation, while others were selectively retained or induced in NPCs, paralleling changes in enhancer usage and histone modification states. Targeted knockdown of these eRNAs decreased Tdp-43 expression and was accompanied by changes in the expression of pluripotency- and lineage-associated markers, without implying direct control over full differentiation trajectories. These findings uncover a previously unrecognized aspect of Tdp-43 transcriptional regulation and highlight the significance of enhancer dynamics in the epigenetic regulation of TDP-43 expression during early lineage specification.
The molecular basis of ecological adaptation in marine crustaceans remains poorly understood, particularly in non-model species such as the coastal slipper lobster (Crenarctus bicuspidatus). This study presents the first comprehensive analysis of the mitochondrial genome and transcriptome of C. bicuspidatus using high-throughput sequencing. Comparative transcriptomic analysis across 13 crustacean species identified 250 single-copy orthogroups. Gene family evolution analysis revealed 28 gene family expansions and 152 contractions in C. bicuspidatus. KEGG enrichment analysis of the expanded gene families showed strong representation of energy-related pathways, particularly pyruvate metabolism. Furthermore, positive selection analysis identified several genes involved in pyruvate metabolism and the citrate cycle (TCA cycle), including specific amino acid substitutions in the pyruvate dehydrogenase complex, a key enzyme in energy conversion. These findings suggest that C. bicuspidatus has undergone coordinated genomic adaptations to enhance energy metabolism, likely to support the high energetic demands of its extended larval development. This study highlights glycolytic adaptation as a key driver of life-history diversification in slipper lobsters.
Tetramethylthiuram disulfide (TMTD), widely used in rubber manufacturing and agriculture, presents occupational inhalation hazards, yet its effects on human lung epithelial cells remain poorly characterized. Here, we investigated TMTD-induced cellular stress responses in A549 lung epithelial cells, focusing on stress granule formation, oxidative stress, and DNA damage. TMTD induced concentration-dependent cytotoxicity, with brief exposure producing effects comparable to continuous exposure, indicating persistent cellular damage. Using live-cell imaging with A549 G3BP1-GFP knock-in cells, we demonstrated that TMTD rapidly triggered SG formation within minutes, accompanied by marked eIF2α phosphorylation. TMTD exposure caused dramatic intracellular ROS accumulation and robust γ-H2AX phosphorylation. Antioxidant rescue experiments using N-acetylcysteine confirmed that oxidative stress directly drives SG formation and DNA damage. Repeated TMTD exposure significantly increased apoptotic cell populations, demonstrating that cells cannot recover from recurrent exposure. Our findings reveal a mechanistic cascade whereby TMTD induces oxidative stress, triggers SG formation as an adaptive response, causes DNA damage, and ultimately leads to apoptosis when cellular stress overwhelms protective mechanisms. This study establishes stress granule formation as a sensitive early biomarker for TMTD exposure and highlights significant respiratory health risks for workers in rubber and agricultural industries, supporting the need for re-evaluation of occupational exposure limits and implementation of stringent protective measures.
Coleoid cephalopods are excellent models for evolutionary and developmental studies due to their centralized nervous system, short life span, and sophisticated sense organs. Arm suckers, essential for predation, manipulation, and locomotion, have been studied in Decapodiformes, but little is known at the cellular and molecular levels. Here, we investigated sucker development in Octopus minor from the embryo to the juvenile stage using morphological, histological, immunostaining, scanning electron microscopy (SEM), in situ hybridization, and transcriptomic analyses. SEM revealed that suckers initially form symmetrically and later become asymmetrical through an embedding process. Histology showed progressive structural differentiation, while immunostaining with acetylated α-tubulin and phalloidin visualized nerve fiber and muscle development. Transcriptome profiling of embryonic stages 12, 14, and 20 identified 2,349 differentially expressed genes (DEGs) linked to arm and muscle development. Among them, Omi-Gata4, Omi-Mef2A, and WNT signaling molecules (Omi-Fzd9, Omi-Wnt2, Omi-Wnt5) exhibited increased expression in arms and developing suckers, consistent with in situ hybridization results. These findings suggest that WNT signaling contributes to sucker muscle development in O. minor, paralleling its conserved role in vertebrates. This study provides new insights into the embryonic morphogenesis of arms and suckers, highlighting the molecular and cellular mechanisms that shape cephalopod appendages.
The Notch signaling pathway is one of the most evolutionarily conserved pathways, playing a crucial role in juxtacrine signaling between adjacent cells. Although previous studies have characterized Notch signaling in diverse models, its function in the lophotrochozoan animals is largely not understood and is only partially identified in early-stage embryos. To address this gap, we reaffirmed the expression of Notch homolog, including downstream components, in the organogenesis of the Glossiphoniid leech, Helobdella austinensis. We analyze the spatial and temporal expression patterns of the Notch receptor (Hau-notch1), ligands (Hau-delta and Hau-jagged), and transcription factors (Hau-hes and Hau-hey) from embryonic stages 8-11. Notch transcripts are expressed in the germinal plate and segmental precursor cells at stage 8, with expression expanding to the somites, ventral and supraesophageal ganglia by stage 9. In organogenesis stages (stages 9-11), Notch components are expressed in the anterior and posterior suckers, proboscis, and ventral ganglia, indicating their role in nerve differentiation. Furthermore, blocking of Notch signaling by DAPT (N-[N-(3, 5-difluorophenacetyl)-l-alanyl]-s-phenylglycine t-butyl ester) leads to the disruption of nerve formation with downregulation of transcription factors (Hau-hes and Hau-hey). Our findings provide insights into the conserved mechanisms of Notch signaling in bilaterian neural development, contributing to a deeper understanding of evolutionary developmental biology.
Exosomes are a type of extracellular vesicles with a diameter of 30-150 nm, formed within multivesicular bodies of late endosomes, and released into the extracellular environment before being taken up by recipient cells. Exosomes transfer bioactive molecules, such as proteins and various RNAs, between cells and thereby influence recipient cell behavior. Among these molecules, long non-coding RNAs (lncRNAs) are not only selectively packaged into exosomes but have also been reported to participate in exosome biogenesis and secretion. Furthermore, they can contribute to cancer development by regulating gene expression through epigenetic mechanisms such as miRNA sponging, protein interactions, and methylation. These mechanisms appear to drive tumorigenesis by altering the tumor microenvironment, including macrophage polarization, immune evasion and suppression, angiogenesis, and lymphangiogenesis-mediated metastasis. In addition, exosomal lncRNAs can be readily detected in serum, highlighting their potential as biomarkers for liquid biopsy-based diagnosis. Finally, exosomal lncRNAs have been reported to contribute to drug resistance in various cancers. Therefore, therapeutic strategies targeting exosomal lncRNAs are expected to improve clinical outcomes in cancer patients.
Non-genuine conservation status updates threaten the trust in Red Listing, but they are necessary building blocks in science. In addition, they often highlight the critical need for basic field research. The Suweon treefrog, Dryophytes suweonensis, is a hylid species long thought to be range-restricted, and assessed as Endangered by the IUCN Red List of Threatened Species. This study aimed at determining the species of individuals encountered during call surveys in 2024 in China, and aimed to determine the areas of suitable habitat for the species. We sequenced the Cytb gene fragment and compared the acoustic properties of some individuals sampled northern China to identify the species. We also built ecological models with MaxEnt to predict suitable habitats and guide future surveys. We genetically confirmed the identity of the population as D. suweonensis, more than 985 km north of the northernmost known locality for the species. The call properties also matched with those of D. suweonensis. The ecological niche models identified a very large area with suitable habitat spanning the northern Chinese plains. The species is not endemic to the Korean Peninsula, occurring in a significantly broader range, and thus, the population size is higher than previously assumed. The species is unlikely to be threatened, and this huge range extension highlights the need for additional field surveys for all amphibian species in the area. Long term, the use of conservation prioritisation tools will highlight conservation needs in the region.
Metabolic dysfunction-associated steatotic liver disease (MASLD) and its advanced inflammatory subtype, metabolic dysfunction-associated steatohepatitis (MASH), are becoming increasingly prevalent liver disorders driven by complex interactions between metabolic stress, immune dysregulation, and fibrotic remodeling. Regulatory T cells (Tregs), traditionally recognized for their immunosuppressive functions, have emerged as key modulators of hepatic inflammation, fibrosis, and systemic metabolic balance. While Tregs can suppress pro-inflammatory immune responses and mitigate liver injury, accumulating evidence highlights their paradoxical roles in liver fibrosis, including the promotion of hepatic stellate cell activation and profibrotic remodeling. This review critically examines the dual and context-dependent roles of Tregs in MASLD and MASH, emphasizing implications for therapeutic intervention. Additionally, we discuss current preclinical strategies aimed at modulating Treg abundance and function, highlighting the challenges and opportunities associated with developing stage-specific therapeutic approaches that consider not only local hepatic effects but also potential systemic metabolic consequences.
Glioblastoma (GBM) is the most aggressive and lethal form of primary brain tumor, characterized by uncontrolled proliferation and invasion into surrounding brain tissue. Mechanical stimulation (MS) in the tumor microenvironment (TME) has been correlated to tumor progression, partly via ATP release. However, the underlying molecular mechanisms remain poorly understood. In this study, we found that transient receptor potential melastatin 3 (TRPM3) channel mediates MS-induced ATP release from GBM cells. Genetic knockdown of TRPM3 significantly attenuated ATP release and suppressed GBM cell invasion, indicating its functional relevance in tumor dissemination. Furthermore, TRPM3 regulated ATP release in a Ca2+-independent manner, suggesting a noncanonical mechanism of mechanosensitive signaling. Consequently, targeting TRPM3 may offer a novel target to reduce the invasion of GBM within the TME.
Cell signaling regulates cell proliferation, survival, and migration, and abnormal kinase activity is often implicated in cancer. Although kinases are key targets for anticancer therapy, drug-induced compensatory signaling and pathway rewiring often drive acquired resistance. These compensatory responses enable tumor cells to maintain proliferation and survival, contributing to acquired drug resistance. In this study, we investigated adaptive responses following the knockout of four specific kinase genes, ERK2, PLK1, PIK3CA, and PAK4, using HCT-116, a human colorectal cancer cell line. Using CRISPR-Cas9, we generated individual knockout cell lines and conducted quantitative proteomic and phosphoproteomic profiling using isobaric tagging and tandem mass tag (TMTs) to evaluate alterations in the signaling landscape. Our integrated analysis quantified 7,531 proteins and 10,877 phosphopeptides, revealing kinase-specific patterns of compensatory signaling. ERK2 knockout was associated with activation of MAPK- and PI3K/AKT-related kinases, whereas PIK3CA knockout induced extensive proteomic remodeling and engagement of pro-survival phosphorylation programs, illustrating distinct modes of signaling network rewiring. Integration of kinase-substrate enrichment analysis (KSEA) with global proteomic data revealed that adaptive kinase activity was largely uncoupled from protein abundance and uncovered a synthetic lethal interaction between ERK2 loss and RPS6KB1 inhibition. Collectively, these findings elucidate how targeted kinase loss drives homeostatic signaling networks in cancer cells. By systemically characterizing cellular-level signaling changes and contextualizing them within known kinase pathways, our results provide insights into synthetic lethality and identify potential therapeutic targets to counteract adaptive resistance to kinase inhibitors.
Mesenchymal stem cells (MSCs) integrate mechanical information from their microenvironment to regulate lineage commitment. Through integrin-based adhesion, cytoskeletal tension, and nuclear deformation, mechanical cues are transduced into intracellular signals via conserved pathways such as integrin-FAK/Src, RhoA-ROCK, and Hippo-YAP/TAZ. These pathways not only regulate chromatin accessibility and transcriptional output but also induce characteristic changes in mechanosensitive microRNAs (miRNAs). Mechanical loading alters miRNA expression programs that modulate focal adhesion assembly, Rho GTPase activity, and SMAD or Wnt signaling, thereby refining the SOX9-centered transcriptional networks that drive MSC chondrogenesis. Physiological mechanical stimuli including dynamic compression, fluid shear, and controlled tensile strain promote chondrogenic differentiation by lowering actomyosin tension, restricting YAP/TAZ nuclear localization, and enhancing SMAD-SOX9 cooperation. Conversely, pathological changes in the pericellular matrix, such as reduced stiffness and increased permeability, disrupt mechanical filtering, impair force transmission, and destabilize cytoskeletal organization. These mechanical defects shift chondrocytes toward high-tension, YAP-active states that suppress matrix gene expression and hinder maintenance of the chondrogenic phenotype. Simultaneously, dysregulation of mechanosensitive miRNAs weakens negative regulation of inflammatory and catabolic pathways, contributing to extracellular matrix degradation and progressive cartilage degeneration. Although numerous mechanosensitive miRNAs have been identified, their mechanistic roles and context-specific regulation remain incompletely defined. A deeper understanding of how miRNAs integrate diverse mechanical cues is essential to elucidate MSC fate transitions and the mechanobiology of cartilage repair. Advances in single-cell mechanobiology, mechanically tunable culture systems, and miRNA-targeted modulation may ultimately yield diagnostic indicators of mechanical imbalance and new therapeutic strategies for restoring cartilage homeostasis.
Quercus infectoria galls (QIG), traditionally used in Asian and Middle Eastern medicine, have shown lipid-lowering activity by reducing cholesterol, triglycerides, and low-density lipoprotein (LDL) levels. However, their role in regulating adipocyte lipid metabolism remains unexplored. This study aimed to evaluate the anti-obesity potential of QIG extract by investigating its regulatory effects on adipogenesis and lipolysis. The regulatory effects of QIG extract on lipid metabolism were investigated using 3T3-L1 adipocytes. The phytochemical profile of the extract was characterized by LC-QTOF-MS, revealing abundant phenolic constituents, including gallic acid, ellagic acid, and various hydrolyzable tannins. Functional assays demonstrated that the extract markedly suppressed lipid accumulation in a dose-dependent manner, achieving a maximum inhibition of 94.52 ± 2.29% without cytotoxicity. Mechanistically, QIG extract induced G1/S cell cycle arrest, suppressed mitotic clonal expansion, and downregulated key adipogenic transcription factors, adipocyte marker genes, as well as lipogenesis-related genes. In mature adipocytes, the extract significantly promoted lipolysis, increasing glycerol release up to 175.55 ± 5.26% of control levels (p < 0.05). In addition, QIG extract-treated adipocytes exhibited reduced intracellular lipid accumulation and smaller lipid droplets, highlighting its capacity to counteract both adipocyte hyperplasia and hypertrophy. Collectively, these findings provide novel mechanistic evidence that QIG extract exerts dual anti-obesity effects by inhibiting adipogenesis and enhancing lipolysis, supporting its potential development as a natural therapeutic candidate for obesity prevention and metabolic disorder management.
