ABSTRACT
Saffron (Crocus sativus L.) is one of the most expensive spices in the world, boasting rich medicinal and edible value. However, the effective development of active natural substances in saffron is still limited. Currently, there is a lack of comprehensive studies on the saffron stigma protein, and the main effect peptides have not been identified. In this study, the total protein composition of saffron stigmas was analyzed, and two main antioxidant peptides (DGGSDYLGK and VDPYFNK) were identified, which showed high antioxidant activity. Then, the stability of two peptides was further evaluated. Furthermore, our results suggested that these two peptides may protect HepG2 cells from H2O2-induced oxidative damage by significantly improving the activity of endogenous antioxidant enzymes and reducing the malondialdehyde (MDA) content. Collectively, we identified two peptides screened from the saffron protein possessing good antioxidant activity and stability, making them promising candidates for use as functional foods, etc., for health promotion. Our findings indicated that proteomic analysis together with peptide identification is a good method for exploitation and utilization of spice plants.
ABSTRACT
From Siraitia grosvenorii, a natural polysaccharide named SGP-1 was discovered, and its purity was determined to be 96.83%. Its structure is a glucan with 4-, 6- and 4,6-linked glucose units. In this paper, the sulfated derivative S-SGP of SGP-1 was prepared by the chlorosulfonic acid method. The sulfated derivatives were analyzed by Fourier transform infrared spectroscopy (FT-IR), gel permeation chromatography (GPC), and scanning electron microscopy (SEM). The degree of substitution (DS) of the polysaccharide is 0.62, and the weight average molecular weight (Mw) is 1.34 × 104 Da. While retaining the morphological characteristics of polysaccharides, S-SGP appeared a large number of spherical structures and strong intermolecular forces. The in vitro activity study of S-SGP showed that the sulfated derivatives had the ability to scavenge DPPH radicals, hydroxyl radicals and superoxide anions, and the scavenging power tended to increase with the increase in polysaccharide concentration. It can inhibit the growth of human hepatoma cells (HepG2), human breast cancer cells (MDA-MB-231) and human non-small cell lung cancer cells (A549) in vitro. In addition, the treatment of A549 cells with sulfuric acid derivatives can decrease the mitochondrial membrane potential, induce apoptosis, and alter the expression of apoptosis-related mRNA and protein.
ABSTRACT
Selenium is an essential microelement involved in various biological processes. Selenium deficiency increases the risk of human immunodeficiency virus infection, cancer, cardiovascular disease, and inflammatory bowel disease. Selenium possesses anti-oxidant, anti-cancer, immunomodulatory, hypoglycemic, and intestinal microbiota-regulating properties. The non-linear dose-response relationship between selenium status and health effects is U-shaped; individuals with low baseline selenium levels may benefit from supplementation, whereas those with acceptable or high selenium levels may face possible health hazards. Selenium supplementation is beneficial in various populations and conditions; however, given its small safety window, the safety of selenium supplementation is still a subject of debate. This review summarizes the current understanding of the health-promoting effects of selenium on the human body, the dietary reference intake, and evidence of the association between selenium deficiency and disease.
ABSTRACT
Eucommia bark contains many bioactive compounds and has anti-hyperlipidemic effects. However, due to the slow growth rate of the plant, there is a limited supply of this resource. Studies have demonstrated that Eucommia leaves contain active ingredients similar to those of Eucommia bark and also have anti-hyperlipidemic effects. It is not currently clear whether Eucommia leaf can be used as a substitute for Eucommia bark. Furthermore, their mechanism of action for anti-hyperlipidemia by improving the structure of the gut microbiota is also unclear. We aimed to determine the composition of the active ingredients in EBE and ELE by HPLC, establish an HFD-induced hyperlipidemia model, and combine fecal microbiota transplantation (FMT) experiments to investigate the mechanism of EBE/ELE anti-hyperlipidemia by modifying the structure of intestinal microbiota, as well as to compare the effects of EBE and ELE. Our results showed that EBE and ELE contained similar active ingredients and significantly alleviated lipid metabolism disorders and blood glucose levels in the HFD-induced hyperlipidemia model. In this study, EBE and ELE significantly reduced the relative abundance of Desulfovibrionaceae and Erysipelotrichaceae and significantly increased the relative abundance of Ruminococcaceae. They also promoted the production of short-chain fatty acids (SCFAs) and activated the gene expression of the SCFA receptors G protein-coupled receptor 41 (GPR41) and GPR43. In addition, EBE and ELE can significantly increase the expression of the fasting-induced adipose factor (Fiaf) gene in the colon and inhibit the secretion of lipoprotein lipase (LPL) in the liver, thereby inhibiting triglyceride (TG) synthesis. They also significantly activate the expression of GPR41 and GPR43 genes in the epididymal fat tissue, leading to reduced lipid accumulation in adipocytes. These effects on the target genes were associated with changes in the abundance of Desulfovibrionaceae, Erysipelotrichaceae, and Ruminococcaceae bacteria in the intestinal microbiota. Thus, regulating the relative abundance of these microbes may serve as prospective targets for EBE/ELE to influence the Fiaf-LPL gut-liver axis and the SCFAs-GPR41/GPR43 gut-fat axis. In addition, there was no significant difference in the anti-hyperlipidemic effects of ELE and EBE, suggesting that Eucommia leaf may be a suitable alternative to Eucommia bark for managing hyperlipidemia by regulating the structure of the intestinal microbiota. These findings suggest that Eucommia leaves have great potential for development as a functional food with lipid-lowering properties.
ABSTRACT
BACKGROUND: The bark of Eucommia ulmoides (a perennial deciduous tree termed eucommia hereafter) has anti-hyperlipidemia effects due to its bioactive components. However, the slow growth of eucommia bark leads to a deficit in this resource. Studies have shown that eucommia leaf has bioactive components similar to those of eucommia bark and anti-hyperlipidemia effects. At present, the strength of the anti-hyperlipidemia effect of eucommia bark and eucommia leaf has not been reported. Their interaction with the gut microbiota and the mechanism by which the gut microbiota exerts anti-hyperlipidemia effects are unclear. PURPOSES: Through fecal microbiota transplantation (FMT) experiments, this study aimed to investigate the mechanism by which fecal bacteria suspensions containing chlorogenic acid (CGA), eucommia bark extract (EBE), and eucommia leaves extract (ELE) improve high-fat diet (HFD)-induced lipid metabolism disorders. Difference in anti-hyperlipidemia effects between EBE and ELE and exploring an eucommia bark substitute to improve the sustainable utilization of eucommia were also evaluated. RESULTS: EBE and ELE contain eight identical bioactive ingredients, and fecal bacteria suspensions containing EBE and ELE significantly improved HFD-induced lipid metabolism disorders and elevated blood glucose levels. The fecal bacteria suspension of healthy mice containing CGA, EBE, and ELE significantly reduced the relative abundance of Erysipelothrichaceae and Ruminococcaceae and promoted short chain fatty acids (SCFAs) production thereby activating the expression of the SCFA. G protein-coupled receptor 43 (GPR43) gene in colon and epididymal fat tissues. In addition, fecal bacteria suspensions of healthy mice containing CGA, EBE, or ELE significantly activated fasting-induced adipose factor (Fiaf) gene expression in colon tissue and inhibited the secretion of lipoprotein lipase (LPL) in liver tissue, thereby inhibiting the synthesis of triglycerides (TG). Changed in the Erysipelotrichaceae and Ruminococcaceae relative abundances were significantly correlated with these target genes. Thus, regulating the abundance of the Erysipelotrichaceae and Ruminococcaceae could serve as a potential target for the role of fecal bacteria suspensions of healthy mice containing CGA, EBE, or ELE in the Fiaf-LPL gut-liver axis and SCFAs-GPR43 gut-fat axis. In addition, regarding HFD-induced lipid metabolism disorders and gut microbiota structural disorders, we found no significant difference between ELE and EBE. CONCLUSIONS: Our FMT experiments evidenced that EBE and ELE improve lipid metabolism disorders by regulating the gut microbiota, providing a new pathway for treating hyperlipidemia using eucommia dietary therapy. There was no significant difference in the anti-hyperlipidemia effects of ELE and EBE; thus, eucommia leaf could replace eucommia bark in traditional Chinese medicine, so as to achieve a sustainable utilization of eucommia resources.
Subject(s)
Eucommiaceae , Gastrointestinal Microbiome , Lipid Metabolism Disorders , Mice , Animals , Diet, High-Fat/adverse effects , Lipid Metabolism , Eucommiaceae/chemistry , Lipoprotein Lipase , Plant Bark , Liver , Fatty Acids, Volatile/metabolism , Plant Extracts/therapeutic use , Lipid Metabolism Disorders/drug therapy , Lipid Metabolism Disorders/metabolismABSTRACT
The inflammatory and antioxidant effects of a novel Siraitia grosvenorii polysaccharide (SGP-1-1) were investigated in an inflammation-suppressed diabetic nephropathy (DN) mouse model, and the underlying molecular mechanisms of inflammation and oxidative stress in SGP-1-1-treated mouse models were elucidated. The results demonstrated that DN mouse models treated with SGP-1-1 (50, 100, and 200 mg kg-1 d-1) exhibited good inflammation-modulating activity. In addition, histopathological analysis showed that glomerular atrophy, severe glomerular thylakoid hyperplasia, tubular endothelial detachment, basement membrane exposure, cytoplasmic infiltration with inflammatory cells, and interstitial oedema were all alleviated in DN mice after treatment with SGP-1-1. Metabolomics analysis based on UPLC-Q-TOF/MS revealed that a close relationship between the occurrence of DN and the potential 39 biomarkers, especially, leukotriene E3 and arachidonic acid,of which the main invloved metabolic pathways may beglycerophospholipid metabolism, arachidonic acid metabolism and primary bile acid biosynthesis. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis results demonstrated that SGP-1-1 downregulates mRNA and the protein expression of the G protein-coupled cell membrane receptor TLR4 and its downstream protein kinase (NF-κB p65). This, resulted in the inhibition of the TLR4-NF-κB pathway in the peritoneum of DN mice by regulating inflammation, while stimulating the production of superoxide dismutase (SOD) and reducing the production of cytokine (IL-6, TNF-α) and malondialdehyde (MDA).
Subject(s)
Antioxidants/therapeutic use , Cucurbitaceae , Diabetic Nephropathies/prevention & control , Polysaccharides/therapeutic use , Animals , Animals, Outbred Strains , Antioxidants/administration & dosage , Antioxidants/pharmacology , Diabetes Mellitus, Experimental , Disease Models, Animal , Male , Mice , NF-kappa B/metabolism , Polysaccharides/administration & dosage , Polysaccharides/pharmacology , Signal Transduction/drug effects , Specific Pathogen-Free Organisms , Toll-Like Receptor 4/metabolismABSTRACT
Cadmium (Cd), a biologically non-essential heavy metal, is widespread in the environment, including the air, water, and soil, and is widely present in foods and quantum dot preparations. Cd enters the body primarily through inhalation and ingestion. Its biological half-life in humans is 10-35 years; therefore, Cd poses long-term health risks. While most studies on Cd toxicity have focused on organ and tissue damage, the immunotoxicity of Cd has drawn increasing attention recently. Cd accumulates in immune cells, modulates the function of the immune system, triggers immunological responses, and leads to diverse health problems. Cd acts as an immunotoxic agent by regulating the activity and apoptosis of immune cells, altering the secretion of immune cytokines, inducing reactive oxygen species (ROS) production and oxidative stress, changing the frequency of T lymphocyte subsets, and altering the production of selective antibodies in immune cells. This review summarizes the immunological toxicity of Cd, elucidates the mechanisms underlying Cd toxicity in terms of innate immunity and adaptive immunity, and discusses potential strategies to alleviate the adverse effects of Cd on the immune system.
Subject(s)
Adaptive Immunity/drug effects , Cadmium Compounds/adverse effects , Environmental Pollutants/adverse effects , Immune System/drug effects , Immunity, Innate/drug effects , Animals , Apoptosis/drug effects , Cytokines/metabolism , Humans , Immune System/immunology , Immune System/metabolism , Immune System/pathology , Oxidative Stress/drug effects , Reactive Oxygen Species/metabolism , T-Lymphocyte Subsets/drug effects , T-Lymphocyte Subsets/immunology , T-Lymphocyte Subsets/metabolismABSTRACT
The preventive effect of lychee pulp phenolics (LPP) on dextran sulfate sodium (DSS)-induced colitis of mice and its underlying mechanisms were investigated in this research. LPP supplementation mitigated DSS-induced breakage of the gut barrier as evidenced by the increased tight junction proteins and the enhanced integrity of epithelial cells. Both LPP and 5-ASA treatments could downregulate the expressions of toll-like receptor 4 (TLR-4), NOD protein-like receptor 3 (NLRP3), and proinflammatory cytokines to normal levels. Notably, treatment with LPP at a dosage of 500 mg/kg/day effectively upregulated FFAR2 and FFAR3 expression and contents of short-chain fatty acids (SCFAs), suggesting the activation of the SCFA-FFAR (free fatty acid receptor) pathway. Consistently, the abundances of probiotic taxa and microbiota (Akkermansia, Lactobacillus, Coprococcus, and Bacteroides uniformis) associated with SCFA synthesis were elevated, whereas harmful bacteria (Enterococcus and Aggregatibacter) were suppressed. These data indicate that LPP ameliorates gut barrier damage, activates the microbiota-SCFA-FFAR signaling cascade, and suppresses the TLR4/NLRP3-NF-κB pathway, and therefore, LPP supplementation could be a promising way to protect the intestinal tract.
Subject(s)
Colitis , Gastrointestinal Microbiome , Litchi , Microbiota , Animals , Anti-Inflammatory Agents/therapeutic use , Bacteroides , Colitis/chemically induced , Colitis/drug therapy , Colitis/genetics , Dextran Sulfate/toxicity , Fatty Acids, Nonesterified , Fatty Acids, Volatile , Mice , Mice, Inbred C57BL , Mice, Inbred NODABSTRACT
Lychee pulp phenolics (LPP) was subjected to four simulated gastrointestinal digestions and colonic fermentation to investigate the changes in its phenolic composition and bioactivities; the fecal metabolic profiles of LPP-fed mice were also elucidated using UHPLC-ESI-QTOF-MS/MS. After simulated salivary, gastric and intestinal digestion, slight increases in phenolic acids and (+)-catechin occurred relative to undigested LPP, whereas other flavonoids showed an opposite trend. Unlike the above-described separate simulated digestions, successive gastrointestinal digestion significantly enhanced the release of phenolic compounds (p < 0.05), gallic acid (413.79%), ferulic acid (393.69%), (+)-catechin (570.27%) and rutin (247.54%). During colonic fermentation, ten detected phenolics were utilized by gut microbes, among which procyanidin B2 (22.35%) was the most degraded. LPP fermentation accelerated the production of short-chain fatty acids (122.79%). The metabolic pathways altered by LPP including unsaturated fatty acid, biotin, and nicotinamide metabolism may be the potential regulatory mechanisms and associated with the integrity of the gut barrier. These findings indicate that LPP may act as a promising candidate to protect gut health.
Subject(s)
Colon/metabolism , Digestion/physiology , Fermentation/physiology , Gastrointestinal Microbiome/drug effects , Litchi/metabolism , Metabolic Networks and Pathways/drug effects , Animals , Feces/microbiology , In Vitro Techniques , Male , Mice , Mice, Inbred C57BL , Models, Animal , Phenols/metabolism , Plant Extracts/metabolismABSTRACT
Lychee pulp is rich in phenolics and has a variety of biological activities. However, the changes in the phenolic profile under heat treatment are unknown. The effect of the heat treatment temperature on commercial varieties (Guiwei and Nuomici) of canned lychee was investigated by comparing samples that were either unheated (UH), underwent 70 °C heat treatment (HT70) or underwent 121 °C heat treatment (HT121) and then were stored at room temperature. The results showed that the total phenolic content (TPC), total flavonoid content (TFC) and antioxidant activity of the UH, HT70 and HT121 samples were significantly decreased after storage at room temperature for 9 d, 13 d and 25 d, respectively. However, the TPC, TFC and antioxidant activity of HT121 canned lychee were still significantly higher than those of the UH and HT70 samples. However, the texture characteristics of the HT121 samples were worse than those of the UH and HT70 samples, and the color of the canned lychee was darker after the HT121 treatment. Nine individual phenolic compounds were detected in the canned lychee by HPLC-DAD. The gallic acid content was increased after HT121 treatment. In particular, (-)-gallocatechin was generated by HT121 thermal processing. However, after storage at room temperature for 9 d, the contents of (-)-gallocatechin in canned Guiwei and Nuomici were decreased by 96.27% and 94.04%, respectively, and (-)-gallocatechin disappeared after 25 d. In summary, the phenolic contents and antioxidant activity of canned lychee are increased by high-temperature treatment.