Search Results (5,481)

Carbon nanotubes (CNTs) serve as exceptional multifunctional supports for metal phthalocyanine (MPc)-based electrocatalysts, effectively addressing the inherent limitations of molecular catalysts such as poor conductivity and aggregation. This review systematically summarizes the recent advances in engineering the interface between MPcs and CNTs to optimize performance in sustainable energy conversion and environmental remediation. We categorize the engineering strategies into three synergistic dimensions: (1) dispersion and modification engineering, introducing the most direct physical anchoring dispersion strategy via non-covalent interactions and targeted modifications to yield highly active catalysts; (2) chemical bonding engineering, in which robust axial coordination or covalent grafting creates stable, well-defined active sites and prevents leaching; and (3) geometric and spatial engineering, which exploits CNTs’ unique curvature, atomic defects, inner cavities and one-dimensional architecture to induce strain, symmetry breaking, and nanoconfinement, thereby steering reaction pathways or to construct conductive nanocomposites. These strategies highlight that CNTs are not merely passive scaffolds but active regulators that geometrically and electronically modulate MPcs. By balancing molecular dispersion, charge transfer, and mass transport, CNT-supported MPcs exhibit superior activity, selectivity, and stability for critical electrochemical reactions, including the oxygen reduction reaction (ORR), CO₂ reduction reaction (CO₂RR), and nitrate reduction reaction (NO₃RR), demonstrating substantial potential for advancing sustainable energy technologies and environmental applications. Full article

Environmental stressors such as heavy metals and pesticides pose significant threats to honeybee health by inducing oxidative stress. Enhancing nutritional supply has emerged as a potential strategy for honeybees to enhance stress resistance. However, the underlying molecular mechanisms remain poorly understood. This study investigated the role of leucine (Leu) in regulating antioxidant responses in honeybees (Apis mellifera L.), with a focus on the involvement of sestrin and the Target of Rapamycin (TOR) signaling pathway. The results showed that Leu supplementation activated the TOR signaling pathway and upregulated sestrin expression, leading to enhanced antioxidant capacity and reduced reactive oxygen species (ROS) levels. Silencing sestrin disrupted antioxidant homeostasis, increased stress susceptibility, and caused midgut damage, confirming its essential role in oxidative stress resistance. Notably, inhibition of TOR did not prohibit the protective effects of Leu, suggesting that sestrin, rather than TOR, serves as a key mediator. Furthermore, Leu fine-tuned antioxidant responses under different stress conditions through sestrin. Overall, this study demonstrates that Leu and sestrin play a central role in maintaining antioxidant homeostasis and provide a theoretical basis for nutritional strategies to improve honeybee health and stress resilience. Full article

Background: The axillary microbiome is a major contributor to body malodor generation through bacterial metabolism of apocrine and eccrine secretions. Dysbiosis of this microbial community, particularly through overgrowth of odorigenic species such as Staphylococcus aureus, is associated with increased volatile compound production and local skin inflammation. Heat-treated postbiotics represent a promising class of cosmetic ingredients combining microbiological safety with retained bioactive properties. Objective: We aimed to evaluate the in vitro safety, molecular mechanisms, antipathogen and anti-inflammatory properties of heat-treated Lacticaseibacillus rhamnosus Skinbac™ SB06, and to assess the antiperspirant and deodorant efficacy of a deodorant spray formulation containing 1% SB06 in a controlled clinical study. Methods: In vitro studies assessed cytotoxicity (MTT/LDH assays), Aquaporin-3 (AQP3) expression, reactive oxygen species (ROS) production, antipathogen activity against Staphylococcus aureus (AlamarBlue assay), cytokine modulation (TNF-α, IL-6, IL-8, IL-23) in Normal Human Epidermal Keratinocytes (NHEK) and Peripheral Blood Mononuclear Cells (PBMCs), and axillary microbiome compatibility against Corynebacterium striatum, Staphylococcus epidermidis, and Staphylococcus hominis by viable plate count (CFU/mL). Clinically, a randomized split-body study (n = 20) evaluated antiperspirant effectiveness by gravimetric sweat collection and deodorant efficacy by expert olfactory panel (Likert 1–5) at 24 and 48 h. Results: In vitro testing confirmed the safety of SB06 (MTT and LDH, both non-significant vs. control). SB06 significantly increased AQP3 expression (+20%, p < 0.001) and significantly reduced ROS production (−48%, p < 0.05). Antipathogen testing showed significant reduction in S. aureus planktonic viability (−7%, p < 0.05). Microbiome compatibility testing on selected axillary-associated strains showed a differential compatibility profile, with the strongest inhibitory effect observed for C. striatum (13% residual viability at T24h, corresponding to 87% inhibition), near-complete preservation of S. epidermidis (92% residual viability at T48h), and a mild reduction in S. hominis (−15% at T48h). Cytokine modulation showed significant IL-8 and IL-23 reduction in NHEK (both p ≤ 0.05) and immunostimulatory activity in PBMCs. Clinically, SB06 reduced sweat production vs. placebo by −21.8% at T24 (p = 0.0009) and −10.0% at T48 (p = 0.0495), with significantly lower odor intensity at both timepoints (median score 3 vs. 4, p < 0.0001). Conclusions: Heat-treated L. rhamnosus SB06 showed a multimodal in vitro profile including antipathogen, anti-inflammatory, antioxidant, and AQP3-upregulating activities, and was associated with statistically significant antiperspirant and deodorant effects in a randomized controlled split-body study. These findings are consistent with SB06 being a functional postbiotic ingredient with potential for deodorant and antiperspirant applications, pending confirmation in larger controlled studies. Full article

Nitric oxide (NO) is a small, highly reactive gaseous signaling molecule that plays diverse and context-dependent roles in microbial physiology and host–microbe interactions. Over the past decade, increasing evidence has revealed the dual nature of NO as both an antimicrobial effector and a signaling mediator involved in microbial stress responses, metabolism, biofilm dynamics, quorum sensing, virulence regulation, and symbiotic interactions. In microbial systems, NO influences adaptation to environmental stress and contributes to mechanisms associated with persistence and antimicrobial resistance. In host organisms, NO functions as a key component of innate immunity while also participating in beneficial interactions involving rhizobia, mycorrhizal fungi, and probiotic microorganisms. Despite its biological significance, accurate detection and quantification of NO remain challenging because of its transient nature, high reactivity, low physiological concentrations, and interference from related reactive oxygen and nitrogen species. Recent advances in biosensing technologies have substantially improved NO detection capabilities through the development of electrochemical, optical, enzyme-based, microfluidic, wearable, and implantable sensing platforms. These innovations are complemented by analytical techniques including electron paramagnetic resonance spectroscopy, mass spectrometry, fluorescence-based imaging, and advanced microscopy, which enhance sensitivity, specificity, and spatiotemporal resolution in complex biological environments. Concurrently, statistical and computational approaches—including sensor calibration models, multivariate analyses, machine learning algorithms, and bioinformatics pipelines—have become increasingly important for extracting biologically meaningful information from NO-related datasets. Unlike previous reviews that primarily focus on either NO biology or sensing technologies, this review integrates current knowledge of NO-mediated microbial physiology and host–microbe interactions with recent developments in biosensor engineering, analytical methodologies, statistical frameworks, and emerging artificial intelligence (AI)-driven data interpretation. We further highlight applications of NO detection in infectious disease diagnostics, antimicrobial screening, probiotic and biofertilizer evaluation, environmental microbiome monitoring, and real-time studies of symbiosis and infection. Finally, future directions including miniaturized sensing platforms, multi-omics integration, AI-assisted analytics, and sensor standardization are discussed. By unifying molecular, analytical, and computational perspectives, this review provides a multidisciplinary framework and roadmap for advancing NO-based research and translational applications across microbial, environmental, and host-associated systems. Full article

Tetrabromobisphenol A mono(2-hydroxyethyl) ether (TBBPA-MHEE) is an important byproduct during the production of tetrabromobisphenol A (TBBPA) and its related derivatives. Although it has been detected in aquatic environments, its in vivo developmental toxicity and underlying mechanisms remain poorly understood. In this study, zebrafish were used as a model organism to evaluate the early developmental toxicity, neurobehavioral toxicity, and candidate molecular responses associated with TBBPA-MHEE. The 96 h median lethal concentration (96 h-LC₅₀) of TBBPA-MHEE for zebrafish embryos/larvae was 1.684 mg/L. Sublethal nominal exposure concentrations (2, 20, and 200 μg/L) caused developmental abnormalities, including reduced body length, pericardial edema, impaired swim bladder development, and significantly inhibited spontaneous motor activity as well as the response to light–dark transition and mechanical stimulation. Transgenic reporter assays further showed shortened motor neuron projections, reduced brain-region fluorescence in Tg(gad1b:mCherry) larvae, and downregulated the expression of neurodevelopment-related genes. Network toxicology analysis suggested that MTOR, SRC, MAPK3, and GSK3B were identified as candidate targets potentially associated with TBBPA-MHEE-induced neurotoxicity, with significant enrichment of the ErbB signaling pathway and possible perturbation of PI3K/Akt/mTOR-related responses. In addition, TBBPA-MHEE exposure increased the accumulation of reactive oxygen species (ROS) in the larval brain and induced inflammatory and apoptotic responses. Quercetin intervention partially alleviated ROS accumulation and inflammation and improved the developmental and motor phenotypes. Collectively, these findings indicate that TBBPA-MHEE induces neurodevelopmental toxicity in zebrafish, possibly associated with altered transcriptional responses related to ErbB signaling and the PI3K/Akt/mTOR axis, accompanied by oxidative stress, inflammatory responses, and apoptosis-related events. Because exposure concentrations were not analytically verified, all treatment levels are reported as nominal concentrations. This study provides experimental evidence for the toxicological assessment and environmental risk evaluation of TBBPA derivative pollutants. Full article

The brown planthopper (BPH, Nilaparvata lugens) is a major insect pest of rice (Oryza sativa L.) causing severe yield losses across Asia. Although the resistance gene OsBph32 from the cultivar Ptb33 enhances BPH resistance, its molecular and physiological mechanisms remain unclear. Here, we investigated its function using OsBph32-overexpressing lines combined with physiological, transcriptomic, and metabolomic analyses. Overexpression of OsBph32 in the susceptible cultivar 9311 significantly increased resistance to BPH, as indicated by reduced plant damage and suppressed insect growth. This was associated with increased reactive oxygen species accumulation and callose deposition, suggesting activation of early defense responses. Multi-omics analyses revealed that OsBph32 is associated with transcriptional changes in genes involved in cell wall biosynthesis, phenylpropanoid metabolism, and carbon metabolism. Metabolomic profiling further showed increased accumulation of flavonoids, phenolamides, and lignin-related metabolites under BPH infestation, together with changes in carbon metabolism and starch accumulation. Collectively, these results suggest that OsBph32 is associated with coordinated changes in structural reinforcement, secondary metabolism, and carbon metabolism during insect attack, which may contribute to enhanced rice resistance and provide new insights into non-NLR-mediated insect defense mechanisms in plants. Full article

As a major occupational hazard, crystalline silica (SiO₂) poses a severe risk of pulmonary toxicity. While the irreversible fibrosis of late-stage silicosis has been extensively studied, the cellular and molecular mechanisms by which SiO₂ reprograms macrophage metabolism to drive early pathogenesis remain poorly understood. To elucidate this early immune-inflammatory response, we combined targeted metabolomics, pharmacological treatments, and nutrient deprivation in murine alveolar macrophages. Our results demonstrate that SiO₂ exposure severely impairs the master antioxidant regulator, nuclear factor erythroid 2-related factor 2 (Nrf2), triggering excessive reactive oxygen species (ROS) accumulation and upregulated glutamine catabolism to drive pro-inflammatory M1 macrophage polarization. We demonstrated that Nrf2 activation with tert-butylhydroquinone (TBHQ) redirected glutamine metabolic flux from pro-inflammatory catabolism to antioxidant anabolism, significantly attenuating SiO₂-induced M1 polarization. Conversely, Nrf2 inhibition via ML385 exacerbated the inflammatory response. Furthermore, introducing a glutamine deprivation (−Gln) model revealed that restricting glutamine availability significantly attenuated the ability of Nrf2 to reverse M1 polarization, suggesting that its immune-protective effects largely depend on an intact glutamine metabolic pathway. Ultimately, our findings underscore the severe risks of silica exposure and identify the Nrf2–glutamine metabolic axis as a promising target, providing novel mechanistic insights and a robust basis for “antioxidant–metabolic” dual-target interventions in early-stage silicosis. Full article

Macrophage extracellular traps (METs) are chromatin-based structures released by activated macrophages and are increasingly recognized as distinct, context-dependent effectors of innate immunity. Although initially described in antimicrobial defense, METs are now implicated in sterile inflammation, autoimmunity, fibrosis, metabolic and vascular injury, organ-specific damage, and cancer. This review integrates dispersed evidence on MET biology across physiological and pathological settings, moving beyond neutrophil-centered interpretations of extracellular trap biology. We summarize the molecular composition, structural heterogeneity, major forms of METosis, and key regulatory pathways, including PAD-dependent chromatin remodeling, reactive oxygen species and calcium signaling, mitochondrial DNA release, extracellular DNA sensing, protease-mediated injury, and macrophage–stromal crosstalk. We also discuss the dual nature of METs as protective structures that can contain pathogens and amplify early innate responses, but also as pathogenic platforms when excessive, persistent, or insufficiently cleared. Overall, current evidence supports METs as functionally versatile macrophage-derived immune structures whose biological effects depend on the stimulus, tissue microenvironment, and disease context. By providing a unified framework, this review highlights the relevance of METs as potential biomarkers and therapeutic targets in inflammatory, fibrotic, vascular, autoimmune, and malignant diseases. Full article

Background/Objectives: Dietary patterns characterized by excess saturated fat intake contribute to obesity, type 2 diabetes, and cardiac metabolic dysfunction. Ceramides, bioactive sphingolipids synthesized in response to nutrient overload, have emerged as key molecular mediators linking dietary lipid composition to alterations in cardiac metabolic signaling. This review aims to integrate current evidence on diet-induced ceramide remodeling and its impact on intracellular pathways regulating cardiac metabolism. Methods: We analyzed experimental and clinical studies investigating the effects of high-fat and Western-type diets on myocardial ceramide synthesis, lipidomic remodeling, and downstream signaling pathways. Evidence from animal models, genetic and pharmacological interventions, nutritional studies, and circulating biomarker analyses was examined to delineate mechanistic and translational insights. Results: Saturated fatty acid excess, particularly palmitate, activates the de novo ceramide synthesis pathway in the myocardium, promoting accumulation of specific ceramide species. This remodeling impairs insulin signaling through Akt inhibition, protein phosphatase 2A activation, and PKCζ-dependent mechanisms, contributing to cardiac metabolic inflexibility. Ceramides further disrupt mitochondrial function by altering electron transport chain activity, increasing reactive oxygen species production, and modulating mitophagy and apoptotic signaling. Lipidomic studies highlight species-specific effects, with C16-ceramides frequently associated with adverse metabolic and cardiovascular outcomes, whereas very-long-chain ceramides may exert distinct functional roles. Circulating ceramide profiles have also been linked to diet-associated cardiovascular risk. Conclusions: Diet-induced ceramide remodeling represents a central molecular axis connecting dietary lipid excess to altered cardiac metabolic signaling. Targeting sphingolipid metabolism through nutritional or pharmacological strategies may offer novel opportunities for preventing and managing diet-associated cardiac dysfunction. Full article

Reducing water-insoluble residues while maintaining sufficient rheological performance remains a key challenge for guar gum-based fracturing fluid thickeners. Natural guar gum (GG) is widely used in fracturing fluids, but its relatively high content of water-insoluble residues can impair permeability and reduce fracture conductivity. In this study, GG was modified by low-substitution etherification using a glycerol ether-based modifier (GMH-1) under mild alkaline reaction conditions to develop a reduced-residue thickener for fracturing fluid applications. The modification conditions were optimized through an L9 orthogonal design combined with single-factor analysis. Under the optimal conditions of 35 °C, 2.0 h, 2.0 wt % NaOH, and 0.2 wt % GMH-1, the modified product (GMGG) exhibited an apparent viscosity of 125.3 mPa·s and a water-insoluble residue content of 5.1% in a 0.6 wt % aqueous solution; in comparison, GG showed a viscosity of 89.3 mPa·s and a residue content of 12.4%. FTIR, UV-Vis spectroscopy, and elemental analysis provided indirect but consistent evidence for low-substitution chemical modification and the introduction of oxygen-containing hydrophilic groups while largely preserving the polysaccharide backbone. GMGG also showed improved rheological and thermal response behavior, suggesting that low-substitution glycerol etherification may provide a feasible route to balance residue reduction and viscosity enhancement. These results indicate the potential of this strategy for designing reduced-residue guar-based thickeners for fracturing fluids, while further molecular-level characterization is still required to determine the exact substitution pattern and mechanism. Full article

Eukaryotic genomic DNA is packaged into chromatin as nucleosomes, where it remains susceptible to reactive oxygen species (ROS) that generate the mutagenic lesion 8-oxo-7,8-dihydroguanine (8oxoG). While 8-oxoguanine DNA glycosylase 1 (OGG1) can initiate repair of 8oxoG base paired with C within the nucleosome core particle (NCP) in a position- dependent manner, it is unknown whether MutY homolog (MUTYH), the DNA glycosylase that excises misincorporated A opposite 8oxoG, can initiate repair of 8oxoG:A base pairs within NCPs. To address this, we combined cryo-EM, molecular dynamics (MD) simulations, and biochemical assays. We determined that MUTYH activity on nucleosomal 8oxoG:A is strongly suppressed, with detectable excision limited to the entry/exit region. Cryo-EM structures at four superhelical locations reveal that 8oxoG adopts the syn conformation and Hoogsteen base pairs with A, as in non-nucleosomal DNA, indicating that lesion presentation is not altered by the histone octamer. MD simulations further reveal that 8oxoG:A base pair dynamics and local DNA backbone perturbations are similar in nucleosomal and non-nucleosomal DNA. Together, these data establish that the NCP sterically excludes MUTYH from 8oxoG:A base pairs, making them largely inaccessible to MUTYH processing. This work ultimately provides mechanistic insight for the elevated G to T transversion rate observed in histone-bound DNA following oxidative stress. Full article

Transition metal oxides constitute an important materials platform for chromic phenomena because their optical response is strongly coupled to the changes in electronic structure, phase state, carrier concentration, and defect chemistry. This review discusses selected transition metal oxide thin films, with emphasis on VO₂ and other vanadium oxides, WO₃, NiO, and TiO₂. The review summarizes the structural and electronic characteristics of these representative oxide systems and highlights the role of phase composition, crystal structure, oxygen non-stoichiometry, and defect chemistry in determining their optical response. The main thin film preparation routes, including pulsed laser deposition, magnetron sputtering, sol–gel and aerosol spray methods, atomic layer deposition, chemical vapor deposition, electrochemical routes, and molecular beam epitaxy, are reviewed with respect their influence on obtained thin films. Particular attention is given to applications in thermochromic VO₂-and electrochromic WO₃/NiO-based smart windows, and transition metal oxide-based gasochromic hydrogen sensors. Key challenges related to transition temperature tuning, luminous transmittance, solar modulation, optical contrast, cycling stability, ion transport and large-area integration are also discussed. Overall this review provides a comparative overview of selected transition metal oxide thin films by connecting material chemistry and physics, thin film preparation technology and functionality. Full article

The weaning period represents a critical developmental window during which the intestinal host–microbiota interaction network in piglets undergoes profound remodeling and becomes highly vulnerable to disruption. Abrupt dietary transition, reduced feed intake, environmental stressors, and pathogen exposure can collectively interfere with gut microbial succession, epithelial barrier maturation, mucosal immune homeostasis, and neuroendocrine regulation, thereby increasing the susceptibility of piglets to post-weaning diarrhea, intestinal inflammation, and growth retardation. Gut microorganisms contribute to intestinal homeostasis by regulating epithelial renewal, barrier function, immune tolerance, inflammatory thresholds, and host metabolic adaptation through diverse microbial-derived signals, including short-chain fatty acids, tryptophan metabolites, bile acid derivatives, and amino acid-derived metabolites. Conversely, the host actively shapes microbial composition, spatial organization, and functional activity through mucins, antimicrobial peptides, secretory immunoglobulin A, intestinal alkaline phosphatase, epithelial oxygen gradients, and genetic factors. Dysregulation of these bidirectional interactions under weaning stress may shift the intestinal ecosystem from a homeostatic state toward dysbiosis and inflammation. In this review, we summarize current knowledge regarding the establishment and succession of the piglet gut microbiota, the molecular mechanisms underlying host–microbiota crosstalk, the disruption of these interaction networks during weaning stress, and the application of multi-omics approaches to decipher causal mechanisms. We further discuss microbiota-targeted nutritional strategies, including probiotics, prebiotics, synbiotics, postbiotics, functional amino acids, trace elements, and bioactive compounds, for improving intestinal health in weaned piglets. This review aims to provide a mechanistic framework for precision nutritional regulation of piglet intestinal health and for the development of antibiotic-alternative strategies in swine production. Full article

Background: Neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS), differ in etiology but share several convergent pathological mechanisms. Pterostilbene (PTR) is a natural stilbene with reported antioxidant, anti-inflammatory, and neuroprotective properties. This study aimed to prioritize putative PTR-associated targets and biological processes potentially relevant to shared neurodegenerative mechanisms. Methods: An integrative in silico workflow combining network pharmacology, protein–protein interaction (PPI) analysis, GO Biological Process (GO BP) enrichment, molecular docking, and molecular dynamics (MD) simulations was applied. GO BP terms were filtered, focused on neurodegeneration- and neuroprotection-related processes, and subjected to REVIGO-based redundancy reduction. Selected targets were further evaluated by docking and 500 ns MD simulations. Results: A total of 181, 165, 128, and 109 shared PTR–disease targets were identified for AD, PD, HD, and ALS, respectively. Redundancy-reduced GO BP analysis indicated associations with neuroinflammation, oxidative stress and reactive oxygen species-related responses, programmed cell death, MAPK/ERK- and PI3K/AKT-related signaling, ion and calcium transport, and lipid-, steroid-, or hormone-associated regulation. PPI topology prioritized SRC, ESR1, and HSP90AA1 as recurrent hub–bottleneck proteins, whereas MD-based structural interpretation focused on ESR1 and HSP90AA1. MD analyses indicated stable PTR interactions with both proteins, with ESR1 showing the most favorable predicted interaction profile. Conclusions: These findings suggest that PTR may interact with shared neurodegeneration-relevant molecular systems, particularly through ESR1- and HSP90AA1-associated mechanisms. However, the results are exclusively computational and should be interpreted as hypothesis-generating, requiring further experimental validation. Full article

Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two main neurodegenerative diseases and cause disability and death in patients worldwide. Neurodegeneration is characterized by a progressive loss of neuronal function and structure, causing enormous impairment in cognitive–motor function. Magnolol and honokiol are isomeric biphenyl neolignans and have exhibited neuroprotective activity in previous studies. Hence, we assessed and compared honokiol, magnolol, and mixtures of honokiol and magnolol in honokiol/magnolol molar ratios of 1:3, 1:1, and 3:1 in terms of their neurotoxicity, using the cell counting kit-8 (CCK-8) assay, and of their neuroprotective effect on intracellular reactive oxygen species (iROS) against amyloid-beta (Aβ)- and 1-methyl-4-phenylpyridinium ion (MPP⁺)-induced neurotoxicity in SH-SY5Y cells, using the 2′,7′-dichlorodihydrofluorescein diacetate (H₂DCF-DA) assay. The results showed that honokiol (H) and magnolol (M) at 0.1 μM and the mixtures of honokiol and magnolol in H/M ratios of 1:3, 1:1, and 3:1 at 0.0001 μM exhibited a significant neuroprotective effect of reducing iROS in SH-SY5Y cells where neurotoxicity was induced by Aβ- and MPP⁺ (p-value with respect to Aβ-treated cells < 0.005 and p-value with respect to MPP⁺-treated cells < 0.0001). Moreover, magnolol and honokiol possess antioxidant properties according to computational molecular analysis with Highest Occupied Molecular Orbital (HOMO)- Lowest Unoccupied Molecular Orbital (LUMO) prediction, 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), 2,2-diphenyl-1-picrylhydrazyl (DPPH), and Ferric Reducing Antioxidant Power (FRAP) assays. The mixtures of honokiol and magnolol exerted synergistic neuroprotective ability at all ratios while showing better antioxidation ability than that of pure magnolol alone but comparable to that of pure honokiol alone. Drug-likeness, Absorption, Distribution, Metabolism, Excretion, and Toxicity (ADMET) prediction, and toxicity profiles showed that both compounds are promising neuroprotective agents and that one of the possible targeting mechanisms is the ROS-mediated oxidative stress pathway. Additional neuronal cell lines and in vivo models are required to determine similar effects or other protective mechanisms involving the neuroprotective ability of honokiol and magnolol. Full article