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1.
Food Funct ; 13(20): 10461-10475, 2022 Oct 17.
Article in English | MEDLINE | ID: mdl-36134474

ABSTRACT

Scope: Atherosclerosis (AS) is the leading cause of ischemic disease. However, the anti-AS effects of astaxanthin and its potential mechanisms remain unclear. This study is aimed to investigate the function of astaxanthin-rich extract (ASTE) on AS and gut microbiota as well as the difference from atorvastatin (ATO) in apolipoprotein E-deficient (ApoE-/-) mice. Methods and results: Wild type (WT) and ApoE-/- mice were divided into seven groups: the low-fat diet (LFD) and high-fat diet (HFD) groups (in both types) as well as three ApoE-/- groups based on HFD added with two doses of ASTE and one dose of ATO, respectively. After 30 weeks of intervention, results showed that ASTE significantly inhibited body weight increase, lipids accumulation in serum/liver, and AS-lesions in the aorta. Furthermore, fundus fluorescein angiography and retinal CD31 immunohistochemical staining showed that ASTE could alleviate the occurrence of AS-retinopathy. H&E staining showed that ASTE could protect the colon's mucosal epithelium from damage. The gas chromatographic and gene expression analyses showed that ASTE promoted the excretion of fecal acidic and neutral sterols from cholesterol by increasing LXRα, CYP7A1, and ABCG5/8 and decreasing FXR, NPC1L1, ACAT2, and MTTP expressions. Remarkably, the ASTE administration maintained the gut barrier by enhancing gene expression of JAM-A, Occludin, and mucin2 in the colon and reshaped gut microbiota with the feature of blooming Akkermansia. Conclusion: Our results suggested that ASTE could prevent AS in both macrovascular and/or microvascular as well as used as novel prebiotics by supporting the bile acid excretion and growth of Akkermansia.


Subject(s)
Atherosclerosis , Gastrointestinal Microbiome , Retinal Diseases , Animals , Apolipoproteins E/genetics , Atherosclerosis/drug therapy , Atherosclerosis/etiology , Atherosclerosis/prevention & control , Atorvastatin , Bile Acids and Salts/pharmacology , Cholesterol/metabolism , Diet, High-Fat/adverse effects , Mice , Mice, Inbred C57BL , Occludin , Retinal Diseases/complications , Sterols/pharmacology , Xanthophylls
2.
Exp Gerontol ; 165: 111863, 2022 08.
Article in English | MEDLINE | ID: mdl-35660419

ABSTRACT

We explored the effect of phlorizin against cholinergic memory impairment and dysbacteriosis in D-galactose induced ICR mice. The control (CON) group, D-galactose model (DGM) group, and three groups (DG-PL, DG-PM, DG-PH) treated with phlorizin at 0.01%, 0.02%, and 0.04% (w/w) in diets were raised for 12 weeks. Supplementing with phlorizin reversed the loss of organ coefficient and body weight caused by D-galactose. The functional abilities of phlorizin on hippocampal-dependent spatial learning and memory, anti-oxidation, anti-inflammation were also observed. Meanwhile, phlorizin intervention upregulated the gene expression of Nrf2, GSH-PX, SOD1, decreased the gene expression of NF-κB, TLR-4, TNF-α, and IL-1ß in the hippocampus, while enhanced the gene expression of JAM-A, Mucin2, Occludin in the caecum. Furthermore, a neurotransmitter of acetylcholine (ACh) was enhanced, while acetylcholinesterase (AChE) activity was inhibited by phlorizin administration. Moreover, phlorizin administration increased short-chain fatty acids (SCFAs) content, and reduced lipopolysaccharides (LPS) levels, which may relate to the rebuilding of gut microbiota homeostasis. Treatment with phlorizin may be an effective intervention for alleviating cognitive decline and gut microbiota dysbiosis.


Subject(s)
Galactose , Gastrointestinal Microbiome , Acetylcholinesterase/metabolism , Animals , Cholinergic Agents , Memory Disorders/chemically induced , Memory Disorders/drug therapy , Mice , Mice, Inbred ICR , Phlorhizin
3.
Food Funct ; 13(11): 6072-6088, 2022 Jun 06.
Article in English | MEDLINE | ID: mdl-35550649

ABSTRACT

Blue honeysuckle rich in anthocyanins can inhibit starch-digesting enzyme activity. This study evaluated the inhibitory effect and mechanism of blue honeysuckle extract (BHE) on glycosidases (α-amylase and α-glucosidase). BHE was a mixed glycosidase inhibitor with an IC50 of 2.36 ± 0.14 and 0.06 ± 0.01 for α-amylase and α-glucosidase, respectively. Fourier transform infrared (FTIR) spectroscopy, multi-fluorescence spectroscopy, and isothermal titration calorimetry (ITC) confirmed that BHE caused the secondary structure change and static fluorescence quenching of glycosidases, and the interaction was an enthalpy-driven exothermic reaction. Molecular docking proved that the main anthocyanin monomers in BHE interacted with glycosidases through hydrogen bonds and van der Waals forces. Moreover, BHE changed the starch structure and prevented starch from being digested by glycosidases. In vivo, BHE and starch-BHE complexes effectively slowed postprandial hyperglycemia. This research provided a theoretical basis for BHE in antidiabetic healthy food research and development.


Subject(s)
Lonicera , alpha-Glucosidases , Anthocyanins , Digestion , Glycoside Hydrolases , Molecular Docking Simulation , Plant Extracts/chemistry , Starch/chemistry , alpha-Amylases , alpha-Glucosidases/chemistry
4.
J Food Sci ; 87(5): 2133-2146, 2022 May.
Article in English | MEDLINE | ID: mdl-35338483

ABSTRACT

This study explored the advantageous effects of purple sweet potato anthocyanin extract (PSPAE) on redox state in obese mice. The normal chow diet (NCD) group, high-fat/cholesterol diet (HCD) group, and three groups based on HCD and added with low, middle, and high dose of PSPAE (PAL, PAM, and PAH) were raised for 12 weeks. High dose of PSPAE treatment decreased the elevations of the body weight by 24.7%, serum total cholesterol by 48.3%, serum triglyceride by 42.4%, and elevated serum activities of glutathione peroxidase by 53.3%, superoxide dismutase by 57.8%, catalase by 75.4%, decreased serum contents of malondialdehyde by 27.1% and lipopolysaccharides by 40.5%, as well as increased caecal total short-chain fatty acid by 2.05-fold. Additionally, PSPAE depressed toll-like receptor 4 (TLR-4), nuclear factor kappa-B (NF-κB), interleukin 6, tumor necrosis factor α, and preserved nuclear factor erythroid-2-related factor 2 (Nrf2) gene expression. Similarly, the protein expression of Nrf2 was enhanced, while TLR-4 and p-NF-κB/NF-κB were depressed by PSPAE treatment. Moreover, PSPAE administration promoted the protection of intestinal barrier function and rebuilt gut microbiota homeostasis by blooming g_Akkermansia, g_Bifidobacterium, and g_Lactobacillus. Furthermore, antibiotic interference experiments showed that the gut microbiota was indispensable for preserving the redox state of PSPAE. These results suggested that PSPAE administration could be an opportunity for improving HCD-induced obesity and the redox state related to gut dysbiosis. PRACTICAL APPLICATION: Purple sweet potato anthocyanin has diverse pharmacological properties. It is applicable for individuals to consume extracts (as pills or other forms) from raw purple sweet potato if they want to improve obesity or redox state.


Subject(s)
Gastrointestinal Microbiome , Ipomoea batatas , Animals , Anthocyanins/metabolism , Anthocyanins/pharmacology , Cholesterol/metabolism , Homeostasis , Ipomoea batatas/metabolism , Mice , Mice, Obese , NF-E2-Related Factor 2/metabolism , NF-kappa B/metabolism , Obesity/drug therapy , Oxidation-Reduction , Plant Extracts/metabolism , Plant Extracts/pharmacology , Toll-Like Receptor 4/metabolism
5.
J Agric Food Chem ; 69(1): 198-211, 2021 Jan 13.
Article in English | MEDLINE | ID: mdl-33350821

ABSTRACT

We explored the effects of dietary supplementation with phlorizin on redox state-related gut microbiota homeostasis in an obesity mouse model. Mice (C57BL/6J) were grouped as follows for 12 weeks: normal chow diet group (NCD), high-fat and cholesterol diet group (HFD), and treatment groups fed with HFD along with three levels of phlorizin. Phlorizin alleviated the hyperlipidemia and redox status and increased the total ccal SCFA content (1.88 ± 0.25 mg/g). Additionally, phlorizin regulated gene expression related to lipid metabolism, redox status, and cecum barrier and rebuilt gut microbiota homeostasis. After interference by antibiotics, the total phloretin content in the feces was decreased about 4-fold, and most of the health-promoting effects were abolished, indicating that phlorizin might be susceptible to microbial biotransformation and that microecology is indispensable for maintaining the redox state capacities of phlorizin. Phlorizin treatment could be an advantageous option for improving HFD-related obesity and redox states related to gut microbiota homeostasis.


Subject(s)
Gastrointestinal Microbiome/drug effects , Malus/chemistry , Obesity/drug therapy , Phlorhizin/administration & dosage , Plant Extracts/administration & dosage , Animals , Diet, High-Fat/adverse effects , Dietary Supplements/analysis , Homeostasis , Humans , Male , Mice , Mice, Inbred C57BL , Obesity/etiology , Obesity/metabolism , Obesity/microbiology , Oxidation-Reduction/drug effects
6.
Mol Nutr Food Res ; 64(8): e1900876, 2020 04.
Article in English | MEDLINE | ID: mdl-32050056

ABSTRACT

SCOPE: This study explores the beneficial effects of dietary supplementation of black rice anthocyanin extract (BRAE) on cholesterol metabolism and gut dysbiosis. METHODS AND RESULTS: C57BL/6J mice are grouped into the normal chow diet group (NCD), the high-fat and the cholesterol diet group (HCD), and three treatment groups feeding HCD supplemented with various dosage of BRAE for 12 weeks. Results reveal that BRAE alleviates the increased body weight, serum triglyceride (TG), total cholesterol (TC), non-high-density lipoprotein cholesterol levels (non-HDL-C), and increased fecal sterols excretion and caecal short-chain fatty acids (SCFAs) concentration in HCD-induced hypercholesterolemic mice. Moreover, BRAE decreases hepatic TC content through the fundamental regulation of body energy balance gene, adenosine 5'-monophosphate activated protein kinase α (AMPKα). Meanwhile, BRAE improves the genes expression involved in cholesterol uptake and efflux, and preserves CYP7A1, ATP-binding cassette subfamily G member 5/8 mRNA expression, and the relative abundance of gut microbiota. Additionally, the antibiotic treatment experiment indicates that the beneficial effects of BRAE in reducing hypocholesterolemia risk largely depends on the gut microbiota homeostasis. CONCLUSION: BRAE supplement could be a beneficial treatment option for preventing HCD-induced hypocholesterolemia and related metabolic syndromes.


Subject(s)
Anthocyanins/pharmacology , Cholesterol/metabolism , Dysbiosis/diet therapy , Oryza/chemistry , Plant Extracts/pharmacology , Animals , Anthocyanins/analysis , Anthocyanins/pharmacokinetics , Anti-Bacterial Agents/adverse effects , Anticholesteremic Agents/pharmacology , Cholesterol/adverse effects , Cholesterol/genetics , Diet, High-Fat/adverse effects , Dietary Supplements , Dysbiosis/microbiology , Eating/drug effects , Gastrointestinal Microbiome/drug effects , Gene Expression Regulation/drug effects , Intestines/drug effects , Intestines/pathology , Liver/drug effects , Liver/metabolism , Male , Mice, Inbred C57BL , Plant Extracts/chemistry , Sterols/pharmacokinetics
7.
Int J Biol Macromol ; 138: 846-853, 2019 Oct 01.
Article in English | MEDLINE | ID: mdl-31356939

ABSTRACT

Inhibition the activity of glycosidase is an effective method for the treatment and prevention of diabetes. In this study, enzymatic kinetics, fluorescence spectrum experiment, starch granule digestion, molecular docking studies and animal's studies were used to investigate the interaction mechanism of carnosic acid against two glycosidase (α-amylase and α-glucosidase). Enzymatic kinetics showed that carnosic acid inhibited α-amylase activity in a competitive manner and α-glucosidase activity in a non-competitive manner. The half inhibitory concentrations (IC50) of carnosic acid to α-amylase and α- glucosidase were (1.12 ±â€¯0.31) and (0.08 ±â€¯0.17), respectively. The fluorescence quenching experiments showed that the intrinsic fluorescence of α-amylase or α-glucosidase was quenched by forming a complex with carnosic acid, and there was only one binding site between carnosic acid and glycosidase. The starch granules were no longer hydrolyzed by α-amylase after the addition of carnosic acid, which indicated that carnosic acid inhibited the activity of α-amylase. Molecular docking study showed that carnosic acid binds to the amino acid residues of glycosidase through hydrogen bond and van der Waals force, which leads to the change of the molecular conformation of glycosidase and thus reduces the activity of glycosidase. The experiment on mice showed that carnosic acid could effectively reduce postprandial blood glucose in mice.


Subject(s)
Abietanes/chemistry , Abietanes/pharmacology , Glycoside Hydrolase Inhibitors/chemistry , Glycoside Hydrolase Inhibitors/pharmacology , alpha-Amylases/chemistry , alpha-Glucosidases/chemistry , Animals , Blood Glucose/drug effects , Enzyme Activation/drug effects , Kinetics , Mice , Molecular Conformation , Molecular Docking Simulation , Molecular Dynamics Simulation , Spectrum Analysis , Structure-Activity Relationship , alpha-Amylases/antagonists & inhibitors
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