Search Results (11,138)

Introduction: The fruit of the cashew tree, known as cashew, is accompanied by the fleshy extension of its stem, referred to as the cashew nut. Rich in phenolic compounds, such as phenolic acids, anthocyanins, flavonoids, carotenoids, polyphenols, as well as vitamins C and E, the cashew nut exhibits antioxidant properties. Objective: This systematic review investigated the effects of cashew nuts on oxidative stress in rats. Methodology: The study followed PRISMA guidelines and was registered in PROSPERO. Searches were conducted in the Medline (PubMed), EMBASE, BVS, MedRxiv, Science Direct, Scopus, and Web of Science databases. Experimental studies with rats as the target population, evaluating the effects of cashew nut supplementation on oxidative stress, antioxidant enzymatic activities, and inflammatory markers, were included. Exclusion criteria comprised dissertations, reviews, expert opinions, duplicates, and preprints. Results: Five studies published between 2018 and 2022 were included, all utilizing cashew nut supplementation as the intervention. The results demonstrated a significant reduction in oxidative stress, an increase in the activity of antioxidant enzymes, such as SOD and catalase, and a decrease in inflammatory markers, including TNF-α and IL-1β. The most effective dose was 100 mg/kg/day, yielding consistent results across studies. Conclusion: Cashew nuts show potential for reducing oxidative stress, mitigating inflammation, and enhancing antioxidant defenses in rats. However, further clinical studies are required to better explore their benefits in humans, a field that remains less studied compared to other types of nuts. Full article

Amburana cearensis is a plant native to Brazil used in folk medicine for the treatment of several pathological conditions including stroke. Previous research indicates that a dichloromethane extract of A. cearensis seeds (EDAC), rich in coumarins, protects neural cells against oxygen and glucose deprivation (OGD) and glutamate-induced stress. However, further studies are needed to elucidate the role of coumarin, in the protective effect of EDAC. Glutamatergic excitotoxicity is an important cause of neuronal loss involved in the pathogenesis of Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and ischemic stroke. Therefore, this study aimed to investigate the protective effects of coumarin isolated from EDAC against glutamate excitotoxicity in regulating MAPK pathway proteins and reactive oxygen species (ROS) production on PC12 cells. Furthermore, we aimed to investigate the protective effects of coumarin against cell death induced by OGD. We characterized the isolated compound from EDAC as coumarin by ¹H and ¹³C-NMR. Thus, PC12 cells were exposed to OGD or glutamate (20 mM) and/or treated with EDAC or coumarin (500 μg/mL) for 24 h. Subsequently, cell viability was assessed by propidium iodide staining or by MTT test. Furthermore, the expression of MAPK pathway proteins was investigated by Western blot analysis and the expression of cleaved caspase-3 by immunofluorescence. Furthermore, reactive oxygen species (ROS) production was assessed by 2′,7′-dichlorofluorescein diacetate and CellROX. We observed that EDAC and coumarin were able to protect PC12 cells against OGD conditions. Moreover, EDAC totally inhibited the glutamate toxicity in PC12 cells. Meanwhile, coumarin mitigated the glutamate toxicity. Both were able to downregulate the expression of ERK1/2 and phosphorylated ERK and inhibit caspase-3 activation. EDAC and coumarin also prevented the increase of ROS induced by treatment with H₂O₂ or glutamate. Our results evidenced that coumarin from A. cearensis is antioxidative and is an important cytoprotective compound in EDAC against glutamate excitotoxicity or OGD injury. Full article

Zearalenone (ZEA) is a widespread mycotoxin that contaminates cereals and other animal feeds. Sertoli cells (SCs) are the main target of attack by many environmental toxins. Our previous study found that Potentilla anserina L. polysaccharides (PAP-1b) exhibited protective effects against ZEA-induced oxidative damage in testicular SCs. However, the regulatory mechanisms remain incompletely characterized. In this study, SCs were treated with a complete medium (CON group) or medium containing 150 μg/mL PAP-1b (PAP-1b group). After 4 h, 100 μM ZEA was added to the ZEA group and PAP-1b-ZEA group, respectively. Samples were collected after the cells continued to be incubated for 48 h and subsequently subjected to transcriptome sequencing. The results showed that 1018, 7183, and 1023 differentially expressed genes (DEGs) were screened in the CON-vs.-PAP-1b, CON-vs.-ZEA, and ZEA-vs.-PAP-1b-ZEA groups, respectively. Among them, glutathione peroxidase 1 (GPX1) emerges as a key gene within this antioxidant defense mechanism. In addition, these DEGs were significantly enriched in Gene Ontology (GO) terms related to oxidative stress as well as in MAPK and PI3K-AKT signaling pathways, suggesting that PAP-1b effectively mitigated ZEA-induced oxidative damage in SCs by regulating these signaling pathways. These results provide an essential basis for the further elucidation of the role of PAP-1b in mitigating ZEA-induced oxidative damage in SCs. Full article

With rising living standards, the demand for health and nutrition has increased, sparking interest in food antioxidants. Known for neutralizing free radicals, antioxidants protect cells from oxidative damage, potentially aiding in disease prevention and anti-aging. In the food industry, they also enhance preservation and quality. Thus, studying food antioxidant mechanisms, detection methods, and applications holds theoretical and practical value. This review mainly discusses the mechanisms, detection methods, and applications of food antioxidants in nutrition. Firstly, the main research status and development trends of food antioxidants are described. Then, the action mechanisms of food antioxidants are introduced. Food antioxidants can effectively remove free radicals and prevent free radicals from causing damage to human cells, thus delaying aging and preventing disease. Secondly, the methods of detecting food antioxidants are discussed, including liquid chromatography, liquid chromatography–tandem mass spectrometry, gas chromatography, and gas chromatography–mass spectrometry. These methods can be used to analyze antioxidant components in various samples of foods, drugs, plants, etc. Finally, the research progress of plant antioxidants is discussed, including the applications of a variety of highly effective antioxidant components extracted from different plants. This review provides the theoretical basis and application reference for the research of food antioxidants. Full article

Protamine is a promising marine-derived bioactive compound that is highly arginine-rich and has demonstrated unique advantages in medical and biological research. This study, for the first time, investigates the molecular mechanisms underlying the immunomodulatory effects of Salmon Protamine Sulfate (SPS), Symplectoteuthis oualaniensis Protamine (SOP), and its polyethylene glycol (PEG) derivative (SOP-PEG) on RAW264.7 macrophages. The results demonstrate that both SOP and SOP-PEG significantly enhance the proliferation of RAW264.7 cells by promoting the secretion of pro-inflammatory cytokines and nitric oxide (NO), increasing ROS production, and improving antioxidant capacity, in comparison to SPS. Elevated ROS levels play a crucial role in enhancing macrophage immune activity, while the enhanced antioxidant defense mechanisms help maintain redox homeostasis and protect against oxidative stress-induced cellular damage. A Western blot analysis reveals that SOP and SOP-PEG notably regulate the expression of key proteins associated with the PI3K/Akt signaling pathway and anti-apoptotic mechanisms. Furthermore, a flow cytometry analysis indicates a significant increase in the G2/M-phase cell population in the treatment groups, which is corroborated by Western blot data showing alterations in critical regulatory proteins. Notably, SOP-PEG exhibits the strongest effects in regulating macrophage immune activity, which can be attributed to the enhanced stability and prolonged bioactivity resulting from the PEGylation of SOP. This comprehensive study reveals how SOP and SOP-PEG enhance macrophage immune function through multiple mechanisms, including PI3K/Akt activation, redox regulation, and cell cycle modulation. It provides valuable insights and a theoretical foundation for their potential applications in immunotherapy and immune regulation. Full article

Facial nerve injury (FNI) induces complex molecular and cellular responses, with reactive oxygen species (ROS) and free radicals (FRs) playing pivotal roles in nerve degeneration and regeneration. However, to date, no systematic review has specifically investigated the involvement of ROS and FRs in FNI. To address this unmet need, we reviewed the literature on the subject, comprehensively searching SCOPUS, PubMed, Cochrane Library, EMBASE, and Google Scholar to identify studies that assessed the roles of FRs and ROS in FNI and summarize their findings. A total of 15 studies that satisfied search criteria were identified. Key findings showed that excessive ROS and FR lead to mitochondrial dysfunction, lipid peroxidation, and ferroptosis, exacerbating nerve degeneration after facial nerve injury. These effects are modulated by antioxidants, including alpha-lipoic acid, edaravone, N(ω)-nitro-L-arginine methyl ester (L-NAME), glutathione peroxidase 4, glutathione, methylprednisolone sodium succinate, Si-based agents, superoxide dismutase, and tirilazad mesylate. The insights gained from this review suggest that levels of FRs and ROS are strongly associated with the pathophysiology of facial nerve injury and underscore the therapeutic potential of targeting ROS and FR pathways in facial nerve injuries. Full article

Metabolic syndrome (MetS) is a complex cluster of interrelated metabolic disorders that significantly elevate the risk of cardiovascular disease, making it a pressing public health concern worldwide. Among the key features of MetS, dyslipidemia—characterized by altered levels of high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG)—plays a crucial role in the disorder’s progression. This review aims to elucidate the intricate interplay between HDL-C and TG within the context of lipid metabolism and cardiovascular health, while also addressing the detrimental impact of various cardiovascular risk factors and associated comorbidities. The dynamics of HDL-C and TG are explored, highlighting their reciprocal relationship and respective contributions to the pathophysiology of MetS. Elevated levels of TGs are consistently associated with reduced concentrations of HDL-C, resulting in a lipid profile that promotes the development of vascular disease. Specifically, as TG levels rise, the protective cardiovascular effects of HDL-C are diminished, leading to the increased accumulation of pro-atherogenic TG-rich lipoproteins and low-density lipoprotein particles within the vascular wall, contributing to the progression of atheromas, which can ultimately result in significant ischemic cardiovascular events. Ultimately, this paper underscores the significance of HDL and TG as essential targets for therapeutic intervention, emphasizing their potential in effectively managing MetS and reducing cardiovascular risk. Full article

Superoxide dismutase-rich Tetraselmis chuii (T. chuii) is derived from marine microalgae and has been reported to increase gene expression of nuclear factor erythroid 2-related factor 2 (NRF2) and related antioxidant enzymes in myoblast tissue culture models. Human research has indicated that T. chuii supplementation can improve recovery from exercise-induced muscle damage, but its effects on endurance exercise performance and the molecular bases that may underlie any ergogenic effects are unclear. Healthy participants underwent 14 days of supplementation with 25 mg·day⁻¹T. chuii and placebo in a randomized, double-blind, crossover experimental design. Prior to and following each supplementation period, participants completed a high-intensity cycling test to assess time to exhaustion and peak oxygen uptake (${\dot{\mathrm{V}}\mathrm{O}}_{2\mathrm{peak}}$). A resting skeletal muscle biopsy was collected after both supplementation periods to assess gene expression changes. Compared to pre-supplementation values, ${\dot{\mathrm{V}}\mathrm{O}}_{2\mathrm{peak}}$ was increased following T. chuii (p = 0.013) but not placebo (p = 0.66). Fold-change in glutathione peroxidase 7 [(GPX7) 1.26 ± 1.37], glutathione-disulfide reductase [(GSR) 1.22 ± 1.41], glutathione S-transferase Mu 3 [(GSTM3) 1.34 ± 1.49], peroxiredoxin 6 [(PRDX6) 1.36 ± 1.57], extracellular signal-regulated kinase 3 [(ERK3) 1.92 ± 2.42], NRF2 (1.62 ± 2.16), p38 alpha [(p38a) 1.33 ± 1.58] and sirtuin 1 [(SIRT1) 1.73 ± 2.25] gene expression were higher after T. chuii compared to placebo supplementation (p < 0.05). Short-term T. chuii supplementation increased ${\dot{\mathrm{V}}\mathrm{O}}_{2\mathrm{peak}}$ and skeletal muscle gene expression of key enzymatic antioxidants (GPX7, GSR, GSTM3, and PRDX6), signalling kinases (ERK3 and p38a), post-translational regulators (SIRT1), and transcription factors (NRF2) that may protect against cellular stress insults. Full article

Inflammatory bowel disease (IBD), a chronic inflammatory disorder of the gastrointestinal tract, is frequently complicated by extraintestinal manifestations such as functional hyposplenism. Increasing evidence highlights its pathogenesis as a multifactorial interplay of gut dysbiosis, intestinal barrier dysfunction, and dysregulated immune responses. While probiotics, particularly Lactobacillus spp., have emerged as potential therapeutics for IBD, restoring intestinal homeostasis, their systemic immunomodulatory effects remain underexplored. Here, we investigated the protective role of Lactobacillus johnsonii N5 in DSS-induced colitis, focusing on inflammation inhibition and splenic T cell regulation. Pretreatment with L. johnsonii N5 significantly attenuated colitis severity, as evidenced by preserved body weight, reduced disease activity index, and prevention of colon shortening. N5 suppressed colonic pro-inflammatory factors such as TNF-α, Il-1b, Il-6, and CXCL1, while elevating anti-inflammatory IL-10 at both mRNA and protein levels. Transcriptomic analysis of the spleen revealed that N5 mediated the downregulation of inflammatory pathways, including the IL-17 and TNF signaling pathways, as well as the HIF-1 signaling pathway, and modulated the metabolic pathway of oxidative phosphorylation. Flow cytometry analysis demonstrated that N5 rebalanced splenic Treg/Th17 responses by expanding the Treg population and reducing the production of IL-17A in Th17 cells. Notably, Th17-associated IL-17A positively correlated with intestinal pro-inflammatory mediators, emphasizing the role of Th17 cells in driving colitis. In contrast, splenic Treg abundance positively correlated with colonic IL-10 levels, suggesting a link between systemic immune regulation and intestinal anti-inflammatory responses. Our study underscores the therapeutic potential of targeting gut–immune crosstalk through probiotics, thereby offering valuable insights for developing live bacterial-based interventions for IBD and other inflammatory disorders. Full article

The growing prevalence of obesity is being increasingly acknowledged as a major public health issue. This mainly stems from the excessive intake of dietary fats. Dendrobium officinale (DO), recognized as an herb with dual roles of food and medicine, is renowned for its diverse health-promoting effects. Nevertheless, the specifics of its antiobesity and anti-inflammatory properties and the underlying mechanisms are still obscure. The present study shows that treatment with Dendrobium officinale extract (DOE) alleviates obesity, liver steatosis, inflammation, and oxidative stress in rats that are obese due to a high-fat diet (HFD). Firstly, with respect to HFD obese rats, higher doses of DOE significantly reduced TG, TC, LDL-C, blood glucose, and liver AST and ALT, along with lipid droplets. Meanwhile, DOE supplementation significantly reduced oxidative stress induced by ROS and MDA and increased the levels of GSH-Px and SOD in liver tissues. Furthermore, integrated analysis of transcriptomic and microbiomic data revealed that DOE modulated inflammatory responses through the NF-κB/IκB pathway. This regulatory mechanism was evidenced by corresponding changes in the protein expression levels of both NF-κB and IκB. Additionally, DOE was found to modulate gut microbiota composition in obese rats, specifically reducing the relative abundance of Bilophila while increasing beneficial bacterial populations, particularly the genera Akkermansia and Roseburia. These findings suggest that DOE may help retain the homeostasis of the gut microbiota and improve metabolic health by regulating inflammation in the liver and intestine, thereby providing protection against obesity and related metabolic syndromes. Our study demonstrates that DOE, as a natural botanical extract, can effectively facilitate the prevention or treatment of metabolic syndrome through precision dietary interventions. Full article

Lipopolysaccharide (LPS)-induced inflammation impairs sperm function; however, its impact on ejaculated rabbit sperm remains unexplored. This dose-response study aims to determine the LPS concentration that negatively affects sperm motility in vitro, while also providing the first identification of TLR4 localization on rabbit spermatozoa. Additionally, it evaluates malondialdehyde (MDA) levels in seminal plasma as an indicator of oxidative stress. Sperm motility was analyzed using computer-assisted sperm analysis (CASA) after incubation with increasing LPS concentrations (0, 50, 100, 200, 400, 600, and 800 µg/mL) at multiple time points (0, 1, 2, and 4 h). LPS doses ≥ 400 µg/mL significantly reduced progressive and non-progressive motility, as well as curvilinear velocity (all p < 0.001), while increasing the proportion of static spermatozoa (p < 0.05). Receiver operating characteristic (ROC) analysis identified 300 µg/mL as the threshold dose for motility decline. Immunofluorescence revealed TLR4 localization in the midpiece of sperm tails, with weak labeling in control samples and a marked increase after 4 h of incubation with 400 μg/mL LPS. MDA levels were assessed using the thiobarbituric acid reactive substances (TBARS) assay with a colorimetric kit, showing no significant effect of LPS treatment. No correlation was found between MDA and other semen parameters. ccThese findings identify TLR4 on rabbit sperm for the first time and establish a threshold LPS dose for future in vitro studies. Full article

Low-density lipoprotein (LDL) chemically modified by reactive oxygen species (ROS), for example, leaking from red blood cells in the vascular compartment, more readily crosses the vascular endothelium than does nonoxidatively modified LDL to enter tissue fluid. Oxidatively modified LDL (oxLDL) may also be created in the tissue fluid by ROS leaking from cells by design, for example, by inflammatory white cells, or simply leaking from other cells as a consequence of oxygen metabolism. As well as oxLDL, glycatively modified LDL (glycLDL) is formed in the circulation. High-density lipoprotein (HDL) appears capable of decreasing the burden of lipid peroxides formed on LDL exposed to ROS or to glucose and its metabolites. The mechanism for this that has received the most attention is the antioxidant activity of HDL, which is due in large part to the presence of paraoxonase 1 (PON1). PON1 is intimately associated with its apolipoprotein A1 component and with HDL’s lipid domains into which lipid peroxides from LDL or cell membranes can be transferred. It is frequently overlooked that for PON1 to hydrolyze lipid substrates, it is essential that it remain by virtue of its hydrophobic amino acid sequences within a lipid micellar environment, for example, during its isolation from serum or genetically modified cells in tissue culture. Otherwise, it may retain its capacity to hydrolyze water-soluble substrates, such as phenyl acetate, whilst failing to hydrolyze more lipid-soluble molecules. OxLDL and probably glycLDL, once they have crossed the arterial endothelium by receptor-mediated transcytosis, are rapidly taken up by monocytes in a process that also involves scavenger receptors, leading to subendothelial foam cell formation. These are the precursors of atheroma, inducing more monocytes to cross the endothelium into the lesion and the proliferation and migration of myocytes present in the arterial wall into the developing lesion, where they transform into foam cells and fibroblasts. The atheroma progresses to have a central extracellular lake of cholesteryl ester following necrosis and apoptosis of foam cells with an overlying fibrous cap whilst continuing to grow concentrically around the arterial wall by a process involving oxLDL and glycLDL. Within the arterial wall, additional oxLDL is generated by ROS secreted by inflammatory cells and leakage from cells generally when couplet oxygen is reduced. PON1 is important for the mechanism by which HDL opposes atherogenesis, which may provide a better avenue of inquiry in the identification of vulnerable individuals and the provision of new therapies than have emerged from the emphasis placed on its role in RCT. Full article

Coenzyme Q10 (CoQ10), a high-value-added nutraceutical antioxidant, exhibits an excellent ability to prevent cardiovascular disease. Here, a novel Cereibacter azotoformans strain, designated YS02, was isolated for its ability to produce CoQ10 and genetically characterized by whole genome sequencing (WGS). The CoQ10 biosynthesis and metabolism differences of YS02 under various culture conditions were also systematically investigated. Phylogenetic analysis based on 16 S rRNA genes, along with taxonomic verification using average nucleotide identity (ANI) analysis, confirmed its classification as C. azotoformans. Enzymatic genes dxs, dxr, idi, ubiA, and ubiG were annotated in YS02, which are critical genetic hallmarks for CoQ10 biosynthesis. Under aerobic–dark cultivation, YS02 grows well, and CoQ10 production can reach 201 mg/kg. A total of 542 small-molecule metabolites were identified from YS02 in aerobic–dark and anaerobic–light cultivation via ultra-high performance liquid chromatography–coupled quadrupole orbitrap high-resolution mass spectrometry (UPLC-Q-Exactive Orbitrap MS). Additionally, 40 differential metabolites were screened through multivariate statistical analysis. Metabolic pathway analysis revealed that the biosynthesis of phenylalanine, tyrosine, and tryptophan might be latent factors influencing CoQ10 production discrepancies within YS02 under both cultural modes. These findings represent new insights into the metabolic mechanism of YS02 and underscore its potential as an alternative strain source for industrial CoQ10 production, enriching the existing resources. Full article

Inorganic polyphosphate (PolyP) is a high-molecular-weight polymer that plays multiple roles in regulating immune responses. However, the specific anti-inflammatory mechanisms of bacteria-derived PolyP are unclear. In the present study, PolyP was extracted from Lactobacillus plantarum (L. plantarum), and the chain length was estimated to be approximately 250 Pi residues. The immune regulatory functions of PolyP were investigated using a lipopolysaccharide (LPS)-induced RAW264.7 cell oxidative stress model, and dexamethasone was used as a positive control. The result revealed that both dexamethasone and PolyP were protective against oxidative stress by inhibiting macrophage M1 polarization and the production of several markers, such as nitric oxide (NO), reactive oxygen species (ROS), inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2. In addition, PolyP suppressed inflammation progression by regulating the production of several cytokines, such as interleukin (IL)-1β, interferon (INF)-γ, tumor necrosis factor (TNF)-α, and IL-6, and inhibited the expressions of inhibitory κB kinase (IKK) α, IKKβ, and extracellular regulated protein kinases 2 (ERK2). Conclusively, PolyP derived from L. plantarum has the ability to protect cells from oxidative stress damage by inhibiting M1 polarization in macrophages. These findings provide insights into the function of PolyP and offer support for the potential application of PolyP in immune-related diseases. Full article

Endothelial dysfunction driven by oxidative and nitrosative stress is a critical factor in the pathogenesis of diabetes-related vascular complications. This study investigated the antioxidant and anti-inflammatory effects of Gymnema inodorum leaf (GiL) extract and its flavonoid constituents, kaempferol and quercetin, on human umbilical vein endothelial cells (HUVECs) exposed to peroxynitrite-induced stress. Peroxynitrite exposure significantly reduced the mRNA levels of antioxidant enzymes (e.g., catalase, glutathione peroxidase 1, superoxide dismutase 1, and superoxide dismutase 2) while increasing the expression of pro-inflammatory cytokines (e.g., tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, interleukin-10, and interleukin-12), ultimately leading to oxidative stress and cellular damage. Treatment with GiL extract reversed these effects by enhancing the defenses of antioxidants through the upregulation of enzymatic mRNA expression and suppressing inflammation via the downregulation of cytokine gene expression. The flavonoid constituents of the extract were identified as the active compounds responsible for these protective effects, with kaempferol and quercetin exhibiting significant free radical scavenging activity and the modulation of inflammatory signaling pathways. High doses of GiL extract showed greater efficacy in restoring cellular homeostasis and preventing oxidative damage. These findings underscore the potential of Gymnema inodorum as a source of bioactive compounds for preventing and managing endothelial dysfunction and other oxidative stress-related complications in diabetes. Full article