Search Results (4,831)

Reducing reliance on supplemental fish oil is central to sustainable aquaculture, but the molecular consequences of replacing it with vegetable oils remain poorly characterized in the juvenile Chinese soft-shelled turtle (Pelodiscus sinensis). We evaluated whether full substitution of the supplemental dietary fish oil (FO) with linseed oil (LO) or soybean oil (SO) compromises hepatic lipid metabolism in Pelodiscus sinensis. Three isonitrogenous and isolipidic diets, sharing identical fish meal and other ingredient bases and differing only in the supplemental lipid (4% FO, LO or SO), were fed to triplicate groups of juvenile turtles (initial body weight 55.0 ± 0.05 g) for 8 weeks. Growth performance, survival, feed conversion ratio, and serum biochemistry were unaffected. However, both vegetable oil diets altered tissue fatty acid composition, raising n-6 PUFA and lowering n-3 LC-PUFA and the n-3/n-6 ratio in liver and muscle (muscle EPA and DHA each decreased by approximately 40%); the SO group additionally exhibited elevated hepatic malondialdehyde, whereas hepatic lipid droplet area and lipid content did not differ significantly among groups. Liver transcriptomic profiling identified 262 (LO vs. FO) and 214 (SO vs. FO) differentially expressed genes, converging on lipid storage and bile acid metabolism. RT-qPCR confirmed the up-regulation of PLIN3, G0S2 and APOF and the down-regulation of CYP7A1. Over 8 weeks, replacement of supplemental FO maintained growth without overt impairment while altering tissue fatty acid profiles and the hepatic expression of key lipid metabolism genes. Full article

Neuroinflammation, driven by microglial activation and oxidative stress, is a key pathological feature of various neurodegenerative diseases. Dendropanax morbifera Léveille (DM) is a medicinal plant known for its diverse pharmacological activities; however, the influence of leaf developmental stage on its neuroprotective potential remains poorly understood. In this study, we compared the phytochemical profiles of young DM (YDM) and mature DM leaves and evaluated their effects on neuronal metabolism and microglia-mediated neuroinflammation. HPLC analysis revealed that YDM contained approximately 2.4-fold higher levels of chlorogenic acid than DM, while DM exhibited higher quercetin content. In differentiated N2A neuronal cells, YDM treatment significantly upregulated the expression of key metabolic and mitochondrial regulators, including PGC-1α, PPARγ, and CPT2, suggesting enhanced mitochondrial and metabolic regulatory signaling related to biogenesis and fatty acid β-oxidation. Under inflammatory conditions, YDM more potently suppressed the secretion of pro-inflammatory cytokines (IL-6 and TNF-α) in LPS-stimulated BV2 microglia compared to DM. Furthermore, in N2A cells treated with BV2-conditioned medium, both extracts effectively mitigated reactive oxygen species production and restored brain-derived neurotrophic factor expression. These findings demonstrate that leaf age is a critical determinant of the phytochemical composition and biological activity of DM. Our results suggest that chlorogenic acid-rich YDM preparations may offer superior therapeutic advantages in targeting neuroinflammatory and metabolic dysregulation in the central nervous system. Full article

Background: Growing evidence suggests that chronic substance use disrupts the gut microbiota composition and function, which can contribute to intestinal dysfunction, systemic inflammation, and gut–brain axis dysregulation. However, current evidence remains fragmented and heterogenous, with most studies focusing on individual substances rather than substance-specific microbial signatures. Objective: Therefore, this systematic review synthesizes recent evidence (2019–2025) to characterize the impact of chronic substance use, including alcohol, nicotine, opioids, cocaine, and methamphetamine, on the gut microbiota composition and functional integrity. Methods: Following the PRISMA 2020 guidelines, a total of 91,421 records were identified before screening through searches conducted across electronic databases and publisher platforms, including PubMed, Web of Science, ProQuest, and BSCOhost, among others. After duplication removal and application of the predefined eligibility criteria, 60 studies were selected for qualitative analysis. Results: The findings revealed an interspecies similarity in which chronic substance exposure generally induced dysbiosis characterized by a depletion of beneficial short-chain fatty acid (SCFA)-producing taxa, such as Lactobacillus, Akkermansia, and Faecalibacterium, alongside the enrichment of opportunistic pathogens such as Escherichia-Shigella. Alcohol emerged as a particularly potent ecological driver, consistently reducing the richness and diversity of the microbial community. Mechanistically, these alterations are linked to impaired intestinal barrier function, increased lipopolysaccharide translocation, and the activation of systemic inflammatory pathways. Furthermore, substance-specific metabolic fingerprints were identified, including disruptions in glutamate pathways for cocaine and trimethylamine N-oxide precursors for methamphetamine. Preclinical evidence from fecal microbiota transplantation and germ-free models suggests that these microbial shifts actively modulate reward sensitivity and neuroplasticity through the gut–brain axis. Conclusion: Collectively, the data presented in this study support a shift from reductionist addiction models toward a systems-level framework, positioning the gut microbiome as a pivotal, modifiable component of addiction biology and a promising target for novel therapeutic interventions. Full article

This study evaluated the effects of dietary supplementation with 5% Zanthoxylumbungeanum leaf (ZBL) on growth performance, slaughter traits, meat quality, caecal microbiota, serum metabolome, and muscle transcriptome in rabbits. A total of 108 male New Zealand rabbits (60 days old) were randomly assigned to two groups (nine replicates/group; six rabbits/replicate) and fed either a basal diet (CON) or a diet in which 5% wheat bran was replaced with 5% ZBL for four weeks. Growth and slaughter performance did not differ (p > 0.05). ZBL reduced drip loss and cooking loss, enhanced antioxidant capacity, reduced specific saturated (C16:0), and unsaturated (C18:1 n-9 cis) fatty acids in leg muscle (p < 0.05), and the nutritional significance of these fatty acid changes remains unclear. ZBL also altered the levels of several volatile and non-volatile compounds in serum and muscle. It increased caecal abundance of norank_f_Lachnospiraceae and Anaerofilum, elevated serum metabolites (oleuropein, 3-coumaric acid), and upregulated meat quality-related genes (NR3C2, PDZRN3) in leg muscle (p < 0.05). Correlation analyses revealed that the observed changes in meat quality were closely associated with alterations in gut microbiota, serum metabolome, and muscle transcriptome. These findings suggest that dietary 5% ZBL does not compromise growth performance and is associated with changes in rabbit meat quality, which is associated with coordinated alterations in the gut microbiota, serum metabolome, and muscle transcriptome. Full article

Background: Kai-Bi-Bu-Fei Decoction (KBD) is derived from the canonical Traditional Chinese Medicine formulas Xuan-Bai-Cheng-Qi and Ma-Xing-Shi-Gan. It has been employed for decades in the treatment of severe pneumonia with significant clinical efficacy. This study aimed to evaluate the protective effects of KBD against influenza virus-induced severe pneumonia in a murine model and to elucidate the underlying molecular mechanisms. Methods: The chemical profile of KBD was characterized using UPLC-Q-TOF-MS. A severe pneumonia model was established in C57BL/6J mice via intranasal infection with influenza A/Puerto Rico/8/34 (H1N1, PR8). Multiple parameters, including 14-day survival rate, body weight, lung index, histopathological changes, viral load, and pulmonary cytokine/chemokine levels, were assessed. Furthermore, multi-omics analyses were integrated to characterize the gut microbiota and metabolic profiles. Fecal microbiota transplantation (FMT) was subsequently performed to validate the functional role of the gut microbiota and its metabolites. Results: KBD treatment significantly improved the survival rate by 40%, reduced the lung index by 27.85%, and alleviated lung injury. It also markedly lowered the viral load by 80.88%, suppressed pro-inflammatory cytokine levels, and restored intestinal barrier integrity. Mechanistically, KBD restored gut microbiota diversity by increasing the abundance of Firmicutes and Bacteroidetes, enriching beneficial genera such as Bifidobacterium and Faecalibaculum, and reducing Verrucomicrobiota. Integrated transcriptomic and metabolomic analyses revealed that KBD enhanced short-chain fatty acid (SCFA) metabolism and up-regulated pyruvate metabolism. Finally, FMT confirmed that the therapeutic benefits of KBD were transferable via the microbiota to microbiota-depleted mice. Conclusions: KBD exerts robust protection against severe influenza pneumonia, a process primarily mediated by the gut microbiota–SCFA axis. The enhancement of mitochondrial energy metabolism also appears to play a critical role in its therapeutic mechanism. Full article

Background/Objectives: Chemotherapy-induced peripheral neuropathy (CIPN) affects up to 85% of patients receiving neurotoxic regimens, often leading to dose reduction and impaired quality of life, yet effective preventive or therapeutic options remain scarce. Emerging evidence implicates chemotherapy-induced gut microbiota dysbiosis in CIPN pathogenesis via a gut–nerve axis. Concurrently, rectal ozone insufflation (ROI) has been shown to modulate the gut microbiota and reduce inflammation in preclinical models. This article critically examines the evidence on the role of gut dysbiosis in CIPN, evaluates the microbiota-modulating capacity of rectal ozone therapy (OT), and assesses the biological plausibility of ozone as a microbiota-targeting intervention for CIPN, while explicitly distinguishing between established evidence and hypothetical mechanisms. Evidence synthesis: Neurotoxic agents induce dysbiosis marked by reduced microbial diversity, loss of short-chain fatty acid-producing bacteria, and expansion of pro-inflammatory taxa. Preclinical models demonstrate a causal role for specific microbial communities in CIPN, with microbiota depletion or fecal transplantation modulating neuropathic phenotypes. In human cohorts, dysbiosis severity correlates with CIPN symptoms. Preclinical studies show that ROI restores microbial balance, enhances short-chain fatty acid levels, and strengthens intestinal barrier function via Nrf2/HO-1 and SIRT1 pathways. Preliminary retrospective data from small case series (n = 7 and n = 15) report sustained symptom improvement in CIPN patients receiving OT. However, no human study has directly linked ozone-induced microbiota changes to clinical outcomes, and the clinical evidence for OT in CIPN remains limited to uncontrolled observations. Conclusions: Convergent preclinical evidence supports a biological rationale for investigating ROI as a microbiota-targeting intervention in CIPN. However, this rationale remains largely hypothetical in the clinical setting. High-quality randomized controlled trials with longitudinal microbiome profiling are urgently needed to establish mechanistic causality and to determine whether the promising preclinical findings translate into clinically meaningful benefits. Until such evidence is available, the framework presented here should be regarded as hypothesis-generating rather than as a basis for clinical practice. Full article

Global food waste management necessitates circular bioeconomy solutions to transform organic residues into high-value nutrients to address nutritional demands. This study investigated the valorization of two abundant waste streams, stale bread and sunflower oil through solid state fermentation using food-grade filamentous fungi. Three strains, Neurospora intermedia, Aspergillus oryzae and Rhizopus oryzae were evaluated for the bioconversion of stale bread. Oil supplementation levels of 10, 20 and 30% (g/100 g dry matter) using both fresh and spent sunflower oil were tested to assess changes in proximate composition, characterizing fungal growth dynamics and mycelial development. Furthermore, modifications in fatty acid profiles and hydrolytic enzyme activities were analyzed to determine species responses to oil source and concentration. The results demonstrated that N. intermedia achieved peak protein levels of 36% (g/100 g) alongside efficient starch catabolism, while 10% fresh oil supplementation induced a significant protein increase (26%) in A. oryzae. Regarding lipid accumulation, 10% spent oil supported higher fat content in R. oryzae (19%) compared to fresh oil (17%). PUFA/SFA ratio reached its maximum in A. oryzae with the highest of 5.91 ± 0.56 under 10% fresh oil. Enzymatic analysis identified A. oryzae as the most efficient lipase producer, reaching a maximum activity of approximately 0.10 U/g at 10% spent oil supplementation. Conversely, R. oryzae lipase activity peaked at 20% supplementation (0.08 U/g), reflecting its high capacity for lipid accumulation. These findings establish a potent bioprocess for upcycling mixed food wastes into enhanced functional ingredients for sustainable food and feed systems. Full article

Cardiometabolic diseases are increasingly understood as disorders involving compartment-specific redox disruption rather than a uniform excess of reactive oxygen species. This narrative review synthesizes evidence for a proposed gut microbiota–mitochondria ferroptosis framework in which dysbiosis-derived lipopolysaccharide, trimethylamine N-oxide, short-chain fatty acids, bile acids, and tryptophan metabolites may modulate mitochondrial reactive species production, antioxidant defenses, iron handling, lipid peroxide detoxification, and inflammatory signaling. The reference set was assembled through searches of PubMed and Web of Science Core Collection, supplemented by targeted Google Scholar searches and citation chaining during manuscript preparation and revision through June 2026 and was organized around microbial metabolites, mitochondrial redox biology, ferroptosis pathways, disease-specific evidence, and redox-targeted interventions. Because this is a narrative synthesis rather than a systematic review, the framework should be interpreted as hypothesis-generating rather than as a systematically validated pathological model. Across atherosclerosis, diabetic cardiomyopathy, metabolic dysfunction-associated steatotic liver disease, obesity-associated insulin resistance, chronic kidney disease, and cardiorenal metabolic injury, the most consistent mechanistic links involve mtROS, impaired mitophagy, glutathione/GPX4 and SLC7A11 dysfunction, ACSL4-dependent lipid peroxidation, Nrf2 signaling, NLRP3 activation, and cGAS-STING-associated inflammation, although human causal evidence remains uneven. Importantly, much of the current literature supports local links within this sequence rather than a fully verified dysbiosis–metabolite–mitochondria ferroptosis–organ dysfunction chain in the same study. We therefore emphasize evidence tiers, terminology discipline, and biomarker requirements when interpreting ferroptosis-sensitive injury. Polyphenols, flavonoids, probiotics, postbiotics, melatonin, CoQ10-related strategies, mitochondria-targeted antioxidants, and ferroptosis-sensitive approaches may be most translatable when paired with microbiome, metabolomic, lipidomic, pharmacokinetic, and redox biomarkers. Full article

Enriching meat with n-3 polyunsaturated fatty acids (n-3 PUFAs) is of considerable nutritional interest because of the well-documented cardioprotective and anti-inflammatory properties of these fatty acids in the human diet. This study investigated the potential effects of dietary Artemisia ordosica Krasch (ARI) supplementation on muscle n-3 PUFA deposition in Albas White Cashmere goats, possibly mediated through the regulation of antioxidant capacity, lipid oxidation, and metabolism. Under the present experimental conditions, ARI supplementation did not significantly affect growth performance, but significantly reduced ruminal C18:0 content (p < 0.05) and increased n-3 PUFA levels (C18:3n3, C22:6n3) in rumen fluid, plasma, liver, and Longissimus dorsi, and the consequent elevation of the muscle PUFA-to-saturated fatty acid ratio (P/S; p < 0.05). Concurrently, ARI supplementation enhanced ruminal and systemic antioxidant capacity, as evidenced by increased glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities, elevated total antioxidant capacity (T-AOC), and upregulated expression of antioxidant-related genes (GSR, GOR, SOD2). Integrated multi-omics analyses revealed that these improvements may be associated with the reduced relative abundance of the core biohydrogenating bacterium s_Butyrivibrio_fibrisolvens and de novo saturated fatty acid synthesis, and potential involvement of the AMPK signaling pathway, with downregulation of FASN; coordinated upregulation of CD36, ACSL3/4, and ELOVL6/7; and upregulation of PPARGC1A, collectively suggesting a promotion of FA oxidation and n-3 PUFA deposition. Collectively, these findings suggest that ARI-promoted n-3 PUFA enrichment in goat meat may be associated with the coordinated modulation of ruminal biohydrogenation, systemic antioxidant capacity, and intermediary lipid metabolism, providing a potential nutritional strategy for developing functional cashmere goat meat. Full article

Background/Objectives: The obesity epidemic coexists with the phenomenon of “hidden hunger” (Type B malnutrition)—a micronutrient deficiency amidst a caloric excess. Traditional dietary assessment methods often distort the actual picture by ignoring technological losses during cooking, which necessitates the use of digital tools. Methods: A cross-sectional study (N = 3267) was conducted using the digital platform “NIAP”. The analysis was based on valid 3–7-day dietary records with algorithmic accounting for nutrient retention factors during thermal processing. The nutrient profiles of individuals with a normal body mass index (BMI) and obesity (BMI ≥ 30 kg/m²) were compared. Results: The epidemiology of intake shortfalls was highly prevalent and pronounced: 99.9% of the cohort had ≥1 inadequacy (with a mean negative deviation of −77.3% for vitamin D and −59.2% for Omega-3), and 61.5% exhibited ≥10 simultaneous multiple intake shortfalls. These inadequacy rates remained robust in a sensitivity analysis excluding under-reporters. The obesity group consumed significantly more energy, saturated fatty acids, added sugars, cholesterol, and sodium, but demonstrated a lower relative macronutrient intake (g/kg of body weight). Absolute fiber intake did not differ between the groups, indicating a decrease in its density per 1000 kcal in the diet of individuals with obesity; the intake of Omega-3 polyunsaturated fatty acids (PUFAs) showed a downward trend. The Na:K ratio was significantly higher in the obesity group (1.19 vs. 1.04, p < 0.001). Correlation analysis confirmed an inverse relationship between BMI and the overall nutrient density of the diet. Conclusions: A high-energy diet does not compensate for systemic micronutrient inadequacy among the evaluated cohort. Obesity is associated with a dietary imbalance favoring “empty calories” and pro-inflammatory components against a background of severe multiple dietary inadequacies. The integration of algorithmic dietary assessment that accounts for cooking losses is critical for objective diagnosis and personalized nutritional intervention. Full article

Saccharomyces cerevisiae yeast products are used to stabilize dairy cattle rumen environments. In this study, multiparous lactating Holstein–Jersey cross cows in late lactation (n = 12; ±150 DIM) were used in a replicated 4 × 4 Latin square design over four 21 d periods to evaluate yeast supplementation on dry matter intake (DMI), milk production, milk components, rumen pH, and redox potential (E_h). A subset of four ruminally cannulated cows were selected for rumen measurements. Treatments included no additive (CON), 14 g yeast culture additive (YCA), 5 g active dry yeast (ADY), and 5 g ADY + 5 g yeast extract additive (YEA) top-dressed once daily. Data were analyzed using GLIMMIX in SAS 9.4, with significance at p ≤ 0.05 and tendencies at p ≤ 0.15. Dry matter intake did not differ among treatments (p > 0.15) but decreased over time (p < 0.05). Milk production, efficiency, lactose, and total solids were not affected (p > 0.15). YCA tended to increase milk fat and fatty acid fractions compared with CON (p < 0.15). Protein in milk was greater in CON (p < 0.05; p < 0.05) than YCA and YEA. Active dry yeast treatments increased the frequency of a buffered rumen (p < 0.05) and promoted a more reducing ruminal environment, characterized by lower redox potential and conditions favorable for anaerobic fermentation (p < 0.05). Overall, supplementing active dry yeasts to dairy cows in late lactation did not affect DMI, production efficiency, or milk quality, but may maintain rumen pH stability. Full article

The present study evaluated the effects of basil essential oil (BEO) and cinnamon essential oil (CEO) on the oxidative stability and fatty acid degradation of vegetable oil blends during deep-frying. Three vegetable oil blends (OB1, OB2, and OB3), formulated with different n-6/n-3 fatty acid ratios, were supplemented with essential oils at concentrations of 200, 400, 800, and 1200 ppm and subjected to repeated deep-frying at 180 ± 5 °C for 8 h with periodic sampling. Changes in fatty acid composition, peroxide value (PV), acid value (AV), malondialdehyde (MDA), and p-anisidine value (AnV) were performed to characterize lipid oxidation under thermal stress. Prolonged frying significantly increased oxidation indices and accelerated the degradation of polyunsaturated fatty acids, particularly n-3 fatty acids, leading to an increased n-6/n-3 ratio. However, supplementation with basil and cinnamon essential oils effectively inhibited lipid oxidation and reduced fatty acid degradation compared with the control. Both essential oils decreased PV, AV, MDA, and AnV in a concentration-dependent manner, with more pronounced effects at 800 and 1200 ppm. Kinetic analysis showed that MDA formation followed a zero-order model, while PV changes fitted a first-order kinetic model, with R2 values ranging from 0.857 to 0.932. These findings suggest that basil and cinnamon essential oils enhance the oxidative stability of vegetable oil blends during deep-frying by reducing lipid oxidation and slowing unsaturated fatty acid degradation, highlighting their potential as natural antioxidants for frying oil applications. Full article

This study aimed to obtain the lipid fraction from cocoa bean husks by applying ethyl acetate as an extraction solvent in an ultrasound-assisted extraction process. The effects of temperature (T), time (t), and solvent:husk ratio (R) on the lipid fraction (LF) yield were evaluated. The removal of minor compounds (phytosterols and tocopherols) and total phenolics was evaluated under selected conditions, as well as the value of conjugated dienes (CDs). Extraction with n-hexane was performed for comparative purposes. The prediction of the solubility of the main compounds identified in the solvents used was conducted. The influence of the variables on LF removal was T > t > R, which provided the highest result (13.54 ± 0.47 wt%) at the highest levels adopted (70 °C, 60 min, 12 g/mL), a value 23% higher than that obtained using n-hexane. Under these conditions, there is also greater recovery of minor compounds from the peels, especially β-sitosterol, which was quantified at 43 to 50% of the concentration of these compounds. The use of ethyl acetate provided greater removal of minor compounds and total phenolics, resulting in lower primary lipid oxidation products (CD value). The relationship between these properties was evidenced by the Pearson correlation matrix, especially for stigmasterol, campesterol, total phenolics, and total minor compounds. The thermodynamic modeling reveals regimes ranging from full miscibility of liquid solutes to limited solubility of phytosterols and gallic acid; however, the contrast with experimental data indicates that real extraction is limited by kinetic barriers and plant matrix effects. The solvent extractor did not influence the fatty acid profile of the LF obtained, consisting mainly of saturated fatty acids (palmitic and stearic). Full article

Background: Cytarabine (Ara-C) remains the cornerstone of remission-induction and consolidation chemotherapy for acute myeloid leukemia (AML) and related hematological malignancies. Despite more than six decades of clinical use, its multi-organ toxicity continues to be managed almost exclusively through dose attenuation and supportive care, with no approved upstream pharmacological prevention strategy available. Objectives: This scoping review aimed to systematically map the breadth and nature of pharmacological agents tested in vivo for their capacity to mitigate cytarabine-induced multi-organ toxicity, to characterize their mechanisms of action and organ targets, and to identify evidence gaps and agents with translational potential. Methods: The review was designed and reported in accordance with the PRISMA-ScR checklist. A structured electronic search was conducted across PubMed/MEDLINE, Scopus, Cochrane Library and Embase, and Web of Science from database inception to 15 July 2025. Eligible studies were restricted to full-text, peer-reviewed, English-language research involving in vivo mammalian models administered cytarabine as the principal toxin, with at least one pharmacological co-intervention and at least one quantitative or histopathological organ-injury outcome. Results: From 5701 retrieved records, 36 eligible in vivo mammalian studies (spanning 1964–2024) were identified. Included studies addressed neurotoxicity (n = 6), gastrointestinal mucositis (n = 9), ocular toxicity (n = 3), hepatotoxicity (n = 3), bone marrow suppression (n = 4), chemotherapy-induced alopecia (n = 5), and reproductive and developmental toxicity (n = 4). Five recurring mechanistic strategies were identified across the heterogeneous agents tested: redox buffering (N-acetylcysteine, α-lipoic acid, rutin, swertiamarin, α-tocopherol), mitochondrial preservation (betanin, thymoquinone, vitamin D, sodium zinc dihydrolipoylhistidinate [DHLHZn]), tissue-microenvironment reprogramming (apraglutide, BADGE, plerixafor, short-chain fatty acids, β-glucan), molecular antagonism (deoxycytidine, dCMP), and immunomodulation (lienal peptide, IL-1β, AHCC). Conclusions: This scoping review provides the first systematic cartography of pharmacological mitigation strategies for cytarabine-induced multi-organ toxicity. Five mechanistic pathways converge across eight organ systems, with apraglutide and N-acetylcysteine representing the most clinically translatable candidates. Plerixafor and PPARγ blockade by BADGE constitute high-priority candidates for bone marrow niche protection, while the deoxycytidine antagonism principle warrants formal pharmacokinetic evaluation. The complete absence of cardiotoxicity mitigation data defines the most critical gap for future research. Full article