搜索结果：Plant & cell physiology

Biotechnology has significantly impacted the cosmetics industry, particularly through the incorporation of plant stem cells, which possess regenerative properties beneficial for skincare. This review aims to evaluate the potential benefits and challenges of using plant stem cells in cosmetics, while discussing future directions for their application in skin care products. The review synthesizes existing literature on the regenerative capabilities of plant stem cells, their role in combating aging, promoting skin repair, and providing protection against ultraviolet damage. It also examines biotechnological methods such as plant cell cultures that mitigate issues associated with raw plant materials. Plant stem cells demonstrate self-renewal and differentiation capabilities, crucial for tissue regeneration and skin healing. Despite their advantages, the cosmetic industry faces hurdles including inconsistent terminology, regulatory challenges, high production costs, and the prevalence of marketing strategies lacking clinical validation. While plant stem cell technology offers promising advancements in skincare, the cosmetic industry must address regulatory and validation concerns to ensure consumer safety and product efficacy. Future research should focus on establishing standardized practices and clinical trials to substantiate the claims of stem cell-based products in cosmetics.

The amino acid L-glutamate plays an important role in cell-cell communication, acting as the primary neurotransmitter in the human brain. Glutamate also plays an important signalling role in land plants, enabling long-range signalling in response to wounding1. However, the role of glutamate as an extracellular signalling molecule in unicellular eukaryotes has received far less attention. We find that ionotropic glutamate receptors are widely distributed in unicellular eukaryotes, including many major phytoplankton lineages. Experimental analyses using diatoms, an important lineage of marine and freshwater algae, revealed that low micromolar quantities of extracellular glutamate induce rapid cytosolic Ca2+ elevations, suggesting a sensitive signalling response. The diatom Ca2+ elevations were specific to glutamate, with little or no response to a range of other amino acids. Glutamate sensing was partially disrupted by domoic acid, a toxic analogue of glutamate produced by some harmful diatom species. The cellular role of extracellular glutamate sensing in diatoms remains to be elucidated, although the ability to sense this abundant amino acid may represent a mechanism that allows unicellular eukaryotes to detect wounding of neighbouring cells within a population. Our findings support a widespread role for glutamate as an extracellular signalling molecule in unicellular eukaryotes that likely enabled the emergence of complex glutamate-dependent signalling networks in multicellular organisms.

Plants have long supported human life as medicines and as sources of oxygen and food. Plant resources have played central roles in healthcare including traditional remedies and modern drugs such as aspirin. Recently, attention has shifted beyond small molecules to include higher-order biological structures such as extracellular vesicles (EVs). Plant-derived nanoparticles (pdNPs), obtained from edible plants by mechanical processing, are approximately 100 nm in size, biocompatible, and outperform mammalian EVs due to their safety, oral availability, stability, and low production cost. These features highlight the potential of pdNPs as platforms for drug delivery and therapeutic applications. Our group has focused on grains, legumes, and agro-industrial byproducts such as rice bran as sources of pdNPs. Corn-derived nanoparticles (cNPs) are abundant and enriched in carotenoids including lutein and zeaxanthin. We have demonstrated that cNPs could inhibit colon26 tumor cell growth by inducing G2 arrest and apoptosis, and also activate macrophages, suggesting dual antitumor and immunostimulatory effects. Furthermore, PEGylation improved pharmacokinetics, enhancing tumor accumulation, and therapeutic efficacy after intravenous administration. Rice bran-derived nanoparticles (rbNPs), prepared at high yield from low-value biomass, showed stronger tumor-specific growth inhibition than Doxil®, a clinically used liposomal formulation of doxorubicin, inducing apoptosis in colon26 cells and suppressing peritoneal dissemination in vivo. These findings highlight the potential of rbNPs as sustainable nanomedicines with therapeutic activity and environmental value. In conclusion, pdNPs, particularly cNPs and rbNPs, are cost-effective, safe, and sustainable biomaterials with great potential for advancing cancer therapy, vaccine development, and drug delivery systems.

Plant terrestrialization necessitated overcoming a barrage of stressors.1 Embryophytes (land plants) use an integrated response network to adjust their molecular physiology in response to terrestrial stressors2-one of the important stressors is UV irradiance. The zygnematophytes are the closest streptophyte algal relatives of embryophytes,3,4,5,6 renowned for their UV resilience7,8,9 and key for inferring the UV response toolkit of the earliest embryophytes.10,11 Throughout evolution, specialized metabolism radiated, yielding chemodiverse responses to environmental challenges12,13,14,15 ranging from UV-shielding flavonoids and coumarins to the polymer lignin of tracheophytes16; homologs of the underpinning core pathway occur in streptophyte algae.17 Here, we exposed the zygnematophyte Mesotaenium to UV-B irradiation and profiled its physiological, morphological, transcriptomic, and metabolomic features. After UV-B exposure, the cells showed rapid photophysiological responses and progressively growing terminal vacuoles. Our transcriptome data capture dynamic changes in gene expression in (1) core downstream homologs of phenol metabolic enzymes, photophysiological homeostats, and DNA repair factors and (2) upstream components featuring key homologs of kinase-mediated signaling cascades, as well as light quality and abscisic acid-mediated signaling components. To scrutinize the acclimatory chassis, we created a metabolite feature database specifically for the Mesotaenium metabolome. The metabolome displayed pronounced temporal shifts, with several phenolic features that accumulate along the UV-stress-acclimation kinetics. Overall, we capture chemodiverse responses, including various phenolics such as methoxypsoralen-like derivatives and coumarins. We establish an integrated model for UV responses in the closest algal relatives of embryophytes, illuminating the toolkit that allowed the progenitors of embryophytes to move out of a protective water column.

The field of extracellular vesicles (EVs) has advanced considerably in recent years with new findings stemming from technical improvements in their isolation and characterization, expanding their potential as tools in vaccines, drug delivery, and timely diagnosis using biomarkers. Consequently, a new area of interest has recently gained prominence: the study of changes in EV morphology and their potential involvement in diseases. Using cryo-TEM analysis, a technique that helps preserve the near-natural state of EVs, multiple morphological and structural variants have been demonstrated in isolates from bodily fluids, cell cultures, and cell lines of mammals, as well as some protozoa and plants. In addition to the classic sphere with a lipid bilayer and hyaline content, pleomorphic, tubular and sac-like EVs, with double, multilayered or lamellar membranes, and in some cases, with electrodense content, have been described. Furthermore, several studies have found alterations in the morphological pattern and/or proportions of these morphological variants in diseases associated with cellular or metabolic dysfunction such as Parkinson's and diabetes, as well as in infectious diseases such as Zika virus and prions. Here, we review the key findings that have propelled the field, provide a catalog of the EVs variants identified to date, discuss mechanisms underlying their formation and their potential biological implication in the course of various pathologies, and identify key challenges that need to be addressed. The information analyzed demonstrate that EVs are highly variable structures, not only in their content but also in their morphology, and that this variation could be related to cellular, metabolic, and infectious pathologies. This underscore the need to understand the origin, regulation, and function of each morphological type of EVs, which could lead to their possible use as diagnostic or therapeutic tools in the future. Findings from the last decade using cryo-TEM in bodily fluids demonstrate the existence of morphological and structural variants of extracellular vesicles (EVs).Emerging evidence from microorganisms and plants suggests that this phenomenon may represent a widespread biological process across nature.Changes in EV morphological variants and their proportions have been reported in several diseases involving metabolic and cellular dysfunction, as well as in some infectious diseases.

Non-small-cell lung cancer (NSCLC) is one of the deadliest malignancies in the world. Signal transducer and activator of transcription 3 (STAT3) plays an important role in the progression of NSCLC. Bruceine D is a bioactive quassinoid compound extracted from Brucea javanica, a plant widely used in traditional Chinese medicine. Tests of cell function were performed to observe the effects of bruceine D on human NSCLC cell lines (H460, PC-9, and SKMES-1). Levels of STAT3, phosphorylated STAT3, Survivin, and other apoptosis-related proteins were detected via Western blotting. The binding of bruceine D to STAT3 was examined using molecular dynamics simulations and surface plasmon resonance spectroscopy. The effect of bruceine D on STAT3 nuclear localization was examined by immunofluorescence. Furthermore, the glucose uptake, lactate production, and extracellular acidification rates of NSCLC cells were analyzed to confirm that bruceine D inhibited glycolysis in NSCLC. The efficacy of bruceine D in vivo was evaluated in a mouse xenotransplantation model. Bruceine D significantly reduced the viability of NSCLC cells, promoted apoptosis, and inhibited the growth of tumors in a mouse xenograft model. Bruceine D was found to bind directly to STAT3, inhibiting glycolysis in NSCLC cells. Western blotting results suggested that the antitumor effects of bruceine D might be mediated by the inhibition of the phosphorylation and nuclear translocation of STAT3. Bruceine D exerts a strong inhibitory effect on NSCLC in vitro and in vivo. Bruceine D has potential application prospects in the field of anti-NSCLC therapy.

Breast cancer (BC) is the most prevalent cancer among women, and retrieving the anti-tumor function of the immune system seems a promising treatment approach for its crucial role in combating cancer cells. In this study, we evaluated the impact of a combination therapy containing a TAK1 inhibitor, Takinib (Tak), a metabolic regulator, Metformin (Met), and an immunostimulant, Lentinula edodes mycelia extract (LEME) on enhancing the immune system's anti-tumor activity in BALB/c mice bearing triple-negative breast cancer (TNBC). BALB/c mice were used to induce TNBC tumors and evaluate tumor growth inhibition. The number of CD8+ CD28+ T cells was determined by immunofluorescence assay, the expression of MUC1 protein was assessed by Western blot, while the expression of TOX, NR4A1, and TIM-3 genes was evaluated by real-time PCR in mouse-derived tumor tissues. MTT assay was performed on different BC cell lines to assess cell viability. Molecular docking results revealed significant interactions between Tak and Met with TOX and NR4A1. The combination treatments of Tak, Met, and LEME significantly decreased tumor volume/weight in mice and also significantly increased the number of infiltrated CD8+ CD28+ T cells, reduced MUC-1 protein expression, and decreased the expression of TOX, NR4A1, and TIM-3 genes in mouse tumor tissue. Tak, Met, and their combination significantly decreased the cell viability of different BC cell lines. This study suggests that the Tak-Met-LEME combination treatments may inhibit BC progression by increasing CD8+ CD28+ T cell population in tumor tissue and decreasing tumor progression.

Dermal papilla (DP) cells orchestrate hair follicle growth and cycling by secreting signaling molecules that stimulate follicular epithelial stem cells. The signal peptide CUB-EGF-like domain-containing protein 3 (SCUBE3) was recently identified as a potent anagen stimulator secreted by DP cells. Ageratum houstonianum ethanolic extract (AHE) and its active constituent agerarin exhibit anti-inflammatory properties; however, their effects on hair follicle growth remain unclear. This study aimed to investigate the effects of AHE and agerarin on SCUBE3 expression in primary human DP cells and to elucidate the underlying molecular signaling pathway. Cell viability was assessed by measuring cell confluency. Ex vivo hair growth was analyzed using organ cultures of human hair follicles. Gene and protein expression were determined using reverse transcription-PCR, immunoblot analysis, immunofluorescent staining, tyramide signal amplification-based multiplex immunohistochemistry, and gene promoter-reporter assay in primary human follicle DP cells. In a hair follicle organ culture model, both AHE and agerarin increased the population of the anagen phase and promoted hair shaft elongation. AHE and agerarin significantly upregulated SCUBE3 expression at both the mRNA and protein levels. Mechanistically, AHE and agerarin induced activator protein-1 (AP-1) expression by activating mitogen-activated protein kinase signaling pathways, thereby increasing SCUBE3 gene promoter activity. AHE and agerarin promoted hair follicle growth by upregulating SCUBE3 expression via activation of the MAPK-AP-1 signaling axis. In conclusion, AHE and agerarin may serve as potential therapeutic agents for the prevention and treatment of alopecia (hair loss).

Tricholoma terreum, a mushroom rich in bioactive compounds, exhibits notable antioxidant and anticancer properties. Despite its traditional use, its effects on breast cancer metabolism remain underexplored. Here, we conducted comprehensive phytochemical and volatile organic compound profiling of T. terreum extracts and evaluated their cytotoxicity against MCF-7 breast cancer cells. Using SPME-GC-MS and HPLC, we identified a complex chemical matrix dominated by organic acids (acetic acid, 43.85%) and nitrogen-containing heterocyclics (2-acetylpyridine, 15.19%), alongside significant phenolic acids such as gallic acid and syringic acid. Biological assays indicated that the ethanol extract showed notable cytotoxic effects, reducing MCF-7 cell viability to 3.64% after 72 h, while higher viability was preserved in healthy CCD-1072sk fibroblast cells. Using cell viability assays, flow cytometry, and gene expression analysis, we found that ethanol extracts selectively reduced cancer cell viability, induced G0/G1 cell cycle arrest (71.92%), and promoted apoptosis. Mechanistically, treatment downregulated key nucleotide biosynthesis genes (DHFR, TK1) and the glycolytic enzyme gene (ENO1), while upregulating the oxidative stress response gene SLC7A11 (18.32-fold), suggesting disruption of cancer metabolic pathways. These findings reveal a metabolic reprogramming effect of T. terreum extracts, highlighting their potential as metabolism-targeted agents in breast cancer therapy. Further studies are warranted to validate these effects in vivo and isolate active constituents.

Pancreatic cancer (PC) is one of the most aggressive malignancies of the digestive system, characterized by late diagnosis, resistance to conventional therapies, and poor survival outcomes. Therefore, the development of novel, effective, and targeted therapeutic strategies is urgently needed. This study aimed to evaluate the anticancer potential of Acinetobacter baumannii-derived outer membrane vesicles (OMVs) conjugated with Vaccinium myrtillus extract, a low-toxicity natural compound, against pancreatic cancer cells. For this purpose, V. myrtillus was conjugated with A. baumannii-derived OMVs, and the antimicrobial activity of the conjugate was assessed using disk diffusion, minimum inhibitory concentration, time-kill kinetics, and biofilm inhibition assays. The anticancer effects were investigated by treating PANC-1 pancreatic cancer cells and healthy fibroblast cells with OMVs (50 µg/mL) and increasing concentrations of V. myrtillus (5-250 µg/mL). After 24 h, cell viability and cytotoxicity (MTT, LDH), oxidative stress parameters (TAS, TOS, SOD, GR), PI3K/AKT/PTEN signaling pathway components, apoptotic markers (Annexin V/PI, BAX, Bcl-2, Caspase-8), and inflammatory cytokines (IL-1β, IL-10) were analyzed. The OMV-V. myrtillus conjugate (50 µg/mL OMV +250 µg/mL V. myrtillus) significantly reduced cell viability by approximately 60% through disruption of intracellular redox balance. Elevated oxidative stress triggered apoptotic signaling, approximately increased 50% LDH release, and enhanced inflammatory responses. Especially 50 µg/mL OMV +250 µg/mL V. myrtillus treatment group compared to the control group, which approximately increased to 1-fold IL-1β rate. Furthermore, the 50 µg/mL OMV +250 µg/mL V. myrtillus treatment group showed approximately a 0.75-fold increase in PTEN and BAX gene expression, accompanied by a correlated decrease in AKT and BCL-2 gene expression, compared to the control group. These results suggest that OMV-mediated delivery of V. myrtillus represents a promising synergistic therapeutic approach for treatment-resistant pancreatic cancer.

Expression and stability of immunoglobulins in transgenic plants have been investigated and optimized by accumulation in different cellular compartments as cytosol, apoplastic space and endoplasmic reticulum (ER) as will be discussed in this review. In several cases described the highest accumulation of complete active antibodies was achieved by targeting into the apoplastic space. High-level expression of active recombinant single-chain Fv antibodies (scFv's) was obtained by retention of these proteins in the lumen of the endoplasmic reticulum. This has been shown for leaves and seeds of transgenic tobacco as well as for potato tubers. Transgenic tobacco seeds, potato tubers and tobacco leaves can facilitate stable storage of scFv's accumulated in the ER over an extended (seeds, tubers) or a short (leaves) period of time. The expression of specific scFv's in different plant species, plant organs and cellular compartments offers the possibility of blocking regulatory factors or pathogens specifically. Examples are scFv's expressed in the cytosol and the apoplastic space of transgenic plant cells modulating the infection process of plant viruses and a cytosolically expressed scFv that influenced the activity of phytochrome A protein. The immunomodulation approach has been shown to be also applicable for investigating the action of the phyto-hormone abscisic acid (ABA). High-level accumulation of specific anti-ABA scFv's in the ER of all leaf cells has been used to block the influence of ABA on the stomatal functions. Seed-specific expression of high amounts of anti-ABA-scFv's at a defined time of seed-development induced a developmental switch from seed ripening to vegetative growth. It has been demonstrated that ER retention is essential for the accumulation of sufficient scFv to bind high concentrations of ABA in the transgenic seeds.

Plant-derived extracellular vesicles (PDEV) are emerging as natural nanomedicines for various diseases. Scutellaria baicalensis (S. baicalensis) is a traditional Chinese herb long used to treat intestinal inflammatory bowel disorders (IBD), with its therapeutic effects attributed to bioactive flavonoids such as baicalin and wogonin. However, whether SEV contribute to its anti-inflammatory activity remains unexplored. The assembled multi-component nature of SEV, which carry flavonoids, lipids, proteins, and miRNAs, suggests a potential to exert therapeutic effects against IBD through mechanisms distinct from isolated compounds, with potential advantages in bioavailability and multi-target engagement. We demonstrated that SEV exert potent antioxidant and anti-inflammatory effects in LPS-stimulated RAW264.7 macrophages and Caco-2 intestinal epithelial cells. Moreover, we assessed the therapeutic effects of SEV on dextran sulfate sodium (DSS)-induced IBD in a murine model. In inflamed RAW264.7, SEV modulated the NF-κB/NLRP3 signaling axis to exert anti-inflammatory effects. They scavenged reactive oxygen species (ROS), restored mitochondrial membrane potential, upregulated the anti-inflammatory cytokine IL-10, and suppressed the pro-inflammatory cytokines TNF-α, IL-6, and IL-1β. In Caco-2 intestinal epithelial cells, SEV also repaired intestinal barrier function by restoring expression of the tight junction proteins Zonula Occludens-1 (ZO-1), Claudin-1, and Occludin (OCLN), alongside reduced TNF-α levels. In vivo, SEV accumulated at colonic inflammatory loci to effectively alleviate IBD, as evidenced by improved body weight and increased colon length. This protective effect was mediated through inhibition of the NF-κB/NLRP3 signaling axis in colon tissues, which subsequently restored intestinal barrier integrity by increasing goblet cell numbers, upregulating OCLN proteins, and enhancing Mucin2 (MUC2) secretion, while simultaneously rebalancing inflammatory cytokines through suppression of TNF-α/IL-1β and promotion of IL-10 production. SEV have the potential to protect the colon against DSS-induced colitis by inhibiting the NF-κB/NLRP3 signaling pathway, providing a promising therapeutic candidate for IBD.

Cyclic adenosine monophosphate (cAMP) is a fundamental second messenger involved in diverse signaling pathways across both animals and plants. While the role of 3',5'-cAMP has been extensively characterized, the biological significance of its structural isomer, 2',3'-cAMP, remains largely unexplored, particularly in plants. Here, we show that 2',3'-cAMP and 3',5'-cAMP represent parallel signaling systems in Arabidopsis thaliana, with different enzymatic origins and largely distinct downstream effects. In vitro enzymatic assays show that plant adenylate cyclases (ACs), including AFB5 and HpAC1, produce specifically 3',5'-cAMP from ATP, whereas the TIR domain of protein L7 also catalyzes the formation of 2',3'-cAMP from RNA. Comprehensive multiomics analyses reveal that two isomers elicit distinct yet partially overlapping metabolic, proteomic, and transcriptional response: 2',3'-cAMP activates broad, stress-adaptive gene expression reprogramming, while 3',5'-cAMP fine-tunes responses related to nutrient status and cellular homeostasis. Our findings establish the existence of dual cAMP signaling systems in plants, each with specialized functions and provide insights into the complex regulatory networks governing plant physiology.

Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies worldwide. The therapeutic efficacy of conventional chemotherapeutic agents such as doxorubicin (DOX) is limited by dose-dependent toxicity and the development of drug resistance. Combination strategies incorporating bioactive natural products may enhance anticancer efficacy while enabling dose reduction. The present study aimed to evaluate the potential synergistic cytotoxicity of combining Fenugreek aqueous extract (FAE) with (DOX) against the HepG2 cell line. Phytochemical characterization was performed using UHPLC-QTOF-MS/MS Profiling and HPLC. Cell viability and selectivity were assessed using the SRB assay. Apoptosis, necrosis, autophagy, and cell cycle distribution were analysed by flow cytometry and Western blotting. Drug-drug interaction was evaluated using the Chou-Talalay method. Molecular docking was performed to explore potential interactions between selected FAE constituents and apoptosis- and autophagy-related protein targets. FAE enhanced DOX's cytotoxicity on HepG2 cells, with the interaction ranging from synergistic to additive depending on the concentration ratio. The DOX/FAE combination enhanced cell death through sub-G1 arrest and augmented apoptotic, necrotic, and autophagic responses compared with monotherapies. Western blot analysis demonstrated modulation of the Bax/Bcl-2 ratio and increased LC3-II expression. Docking simulations suggested favourable binding of selected steroidal saponins to Bcl-2 and LC3 proteins. These findings indicate that FAE potentiates DOX-induced cytotoxicity in vitro through modulation of multiple regulated cell death pathways. While the results support the possibility of this combination as a dose-modulating strategy, further validation in additional HCC models and in vivo systems is required.

Histone lactylation, a recently identified post-translational modification, is closely linked to the pathogenesis and progression of malignant tumors, making it a promising therapeutic target for acute myeloid leukemia (AML). Increasing clinical and experimental evidence indicates that elevated serum lactate dehydrogenase (LDH) levels serve as both a diagnostic biomarker and an indicator of poor prognosis in AML, reflecting enhanced glycolytic activity and chemotherapy resistance. Patrinia scabiosaefolia Fisch (PS), a traditional medicinal herb, exhibits broad pharmacological activities, including heat-clearing, detoxifying, antibacterial, antiviral, and antitumor effects. However, the molecular mechanisms underlying its antileukemic activity, particularly in AML, remain insufficiently defined. To elucidate how DEPS exerts therapeutic effects in AML through the HIF-1α-histone lactylation axis, we systematically established the association between DEPS-mediated inhibition of histone lactylation and cellular hypoxia. Lactylation pan-antibody incubation confirmed preliminarily that DEPS significantly inhibits histone lactylation modification. Lactate restoration experiments further demonstrated that DEPS markedly suppresses lactate-induced activation of HIF-1α signaling, reducing downstream metabolic proteins and VEGFA expression. Under hypoxic conditions, AML cells displayed increased proliferation and histone lactylation, both of which were attenuated by DEPS treatment. Sodium L-lactate enhanced the expression of HIF-1α and its downstream effectors (HK2, PDK1, PKM2, GLUT1, LDHA, and VEGFA), whereas subsequent DEPS exposure significantly reversed these changes. Ultimately, DEPS inhibits H3/H4 lysine lactylation, induces G2/M cell-cycle arrest, and promotes apoptosis in THP-1 and HL-60 cells, including doxorubicin-resistant HL-60 cells. Collectively, our findings reveal previously uncharacterized antileukemic mechanisms of DEPS involving suppression of the HIF-1α signaling pathway and histone lactylation. These results highlight the importance of epigenetic regulation in AML and support the therapeutic potential of DEPS in AML treatment and reversal of chemoresistance.

Plant metabolism is essential for coordinating growth, development, and defense under changing environmental conditions. Plants continuously adjust their metabolic pathways to balance resource allocation between growth and immune responses. Under stress, metabolic reprogramming redirects energy and resources toward the production of defense compounds and activation of immune signaling pathways. These changes involve complex interactions among primary metabolism, specialised metabolites, and regulatory networks, including calcium signaling, reactive oxygen species, and phytohormones. Advances in metabolomics and multi-omics technologies have improved understanding of the metabolic control of plant immunity; however, knowledge remains fragmented, and an integrated framework linking metabolism, development, and defense is still emerging. This review examines plant immunometabolism by highlighting the dynamic relationships between metabolic networks and immune functions during development and stress. It discusses pathways that influence growth, stress-induced metabolic shifts linked to defense, and how signaling interacts with metabolism. Progress in metabolomics, transcriptomics, proteomics, and computational modeling that supports systems-level analysis of plant metabolism is also summarized. In addition, potential applications in agriculture and biotechnology, including metabolic engineering, genome editing, and metabolomics-based breeding, are considered in relation to crop resilience. By integrating metabolism, signaling, and systems biology, this review provides a broad perspective on how metabolic reprogramming shapes the growth-defense trade-off in plants and outlines future directions for developing climate-resilient crops.

Inflammatory mediators within the tumor microenvironment contribute to lung cancer progression by enhancing cellular motility and invasive capacity through cytokine-dependent signaling networks. Modulation of these inflammation-associated pathways by dietary bioactive compounds may provide complementary strategies for limiting cancer aggressiveness. Our objective was to examine the inhibitory effects of a cyanidin-3-O-glucoside (C3G)-rich fraction from Kum Akha pigmented black rice (CKAB-P1) on inflammation-stimulated A549 cancer cell progression. CKAB-P1 was obtained through solvent-partition extraction and chemically characterized using the pH differential method and high-performance liquid chromatography. A549 cells were pretreated with CKAB-P1 or C3G, followed by stimulation with conditioned medium predominantly containing IL-6 and IL-1&#x3b2; derived from LPS-exposed THP-1 macrophages (THP-1-CS). Effects on cancer cell migration and invasion were evaluated using wound-healing, Transwell invasion, gelatin zymography, and Western blot analyses. CKAB-P1 contained 106.62 &#xb1; 3.54 mg/g extract of total anthocyanins, with C3G representing the major constituent (59.42 &#xb1; 2.54 mg/g extract). Exposure of THP-1-CS stimulated migration and invasion of A549 lung cancer, and neutralization of IL-6 and IL-1&#x3b2; reduced these pro-migratory effects, confirming cytokine involvement. Treatment with CKAB-P1 (10-40 &#x3bc;g/mL) or C3G (2.5-20 &#x3bc;g/mL) markedly attenuated inflammation-enhanced migration and invasion (p < 0.05). A reduction in MMP-2 and MMP-9 activity, along with decreased expression of invasion-associated protein expressions (uPA, uPAR, and MT1-MMP), was observed. Furthermore, both CKAB-P1 and C3G attenuated phosphorylation of JAK1 and STAT3. These findings suggest that anthocyanin-enriched black rice fraction may limit inflammation-driven A549 lung cancer cell aggressiveness through modulation of the cytokine-driven JAK1/STAT3 signaling cascade, indicating its potential relevance as a bioactive dietary component targeting tumor-associated inflammatory signaling.

Drought-induced senescence is a major cause of maize yield loss. While biostimulant priming improves stress tolerance, its molecular basis is unclear. Here we demonstrate that priming maize with the plant-derived biostimulant AgriPrime Stimulus (APS) delays drought-induced leaf senescence at reproductive-stage, resulting in improved cob weight and yield. Integrated physiological, transcriptomic, metabolomic, and phytohormone analyses revealed that APS priming preserves source leaf functionality by maintaining key metabolic processes. APS-primed drought-stressed leaves showed enrichment of photosynthesis-related genes and elevated levels of tricarboxylic acid cycle intermediates, indicating maintained carbon metabolism. APS priming also strengthened cell wall through the induction of genes involved in cellulose, hemicellulose, pectin, cutin, and wax biosynthesis, with increased structural metabolites such as xylose, mannose, and galactonic acid. Delayed senescence was further supported by enhanced redox homeostasis, with upregulation of antioxidant-related genes including superoxide dismutase (SOD3), peroxidases (PRXs), glutathione S-transferases (GSTs), and ascorbate-associated genes (BX13), together with increased levels of protective metabolites such as proline, trehalose, and myo-inositol. In parallel, APS priming suppressed proteolysis and senescence-associated genes (NYC1, NYE1, SAG39, NAC042). Integration of phytohormone and transcriptomic data further revealed maintained growth-promoting hormones alongside reduced abscisic acid and ethylene biosynthesis. Consistent with this reduced catabolic state, APS-primed leaves accumulated amino acids linked to growth, while unprimed drought-stressed leaves accumulated amino acids related to protein degradation. Collectively, these findings show that APS priming preserves source-sink relationships during drought by maintaining leaf longevity, and strengthening sink support, which improves cob weight under water deficit.

Background/Objectives: To address the limitations of natural curcumin, this study focuses on the functional evaluation of structurally optimized derivatives. We aimed to elucidate structure-activity relationships (SAR) and the stage-specific molecular mechanisms of adipogenesis inhibition using an in vitro cellular assay. Methods: Four novel curcuminoids were synthesized and evaluated in 3T3-L1 preadipocytes against natural curcumin (Curcuminoid I). Efficacy and mechanisms were assessed via cell viability assays, quantitative Oil Red O staining, and time-dependent transcriptional profiling (qPCR/Western blotting) of the KLF family and master regulators. Results: SAR analysis identified Curcuminoid III (symmetric 3,5-dimethoxy-4-hydroxy) as the most potent and safe candidate, whereas Curcuminoid IV exhibited cytotoxicity. Time-course analysis revealed a distinct step-wise inhibition mechanism wherein Curcuminoid III significantly upregulated the differentiation repressor KLF2 at the immediate-early phase. This rapid modulation effectively prevented the subsequent induction of pro-adipogenic factors, including KLF9, KLF15, PPAR&#x3b3;, and C/EBP&#x3b1;, in the mid-stage (3-5 d). Consequently, the expression of the maturation marker aP2 was robustly suppressed by the late stage (5-7 d). Conclusions: The symmetric 3,5-dimethoxy-4-hydroxy substitution pattern appears to confer strong anti-adipogenic activity to Curcuminoid III. Early modulation of the KLF2-PPAR&#x3b3; axis at the onset of differentiation may initiate a cascading inhibitory effect throughout the adipogenic program. These findings highlight the potential of structurally optimized plant-derived bioactive compounds as regulators of metabolic cell fate.