Journal of medicinal food最新文献

Mitochondrial dysfunction affects skeletal muscle (SkM) function and is critical in the etiology of age-related sarcopenia. The sirtuin 1-PGC1α pathway is a key regulator of mitochondrial mass, structure, and function. However, pathway activity decreases with aging. Cacao flavanols show promise in their ability to activate mitochondrial pathways. We evaluated the capacity of the flavanol (+)-epicatechin (+Epi) to stimulate such a pathway and favorably impact mitochondrial and oxidative stress (OS)-associated endpoints in aged SkM. Using 23-month-old male Sprague-Dawley rats, an 8-week oral administration of +Epi (1 mg/kg/day) was implemented, and results were compared versus vehicle-treated controls. Assessments included the nicotinamide adenine dinucleotide (NAD)/sirtuin 1/PGC1α pathway, acetylated proteins levels, mitochondrial function and biogenesis, as well as OS-related endpoints in SkM. +Epi increased the NAD/NADH ratio, activation of sirtuin 1, the deacetylation of nuclear protein content, including that of PGC1α. Also, +Epi induced increases of TFAM and NRF1 mRNA levels, deacetylation of mitochondrial complex I and V, increases in complex I activity, sirtuin 3, complexes I and V, mitofilin, and TFAM protein levels. SkM citrate synthase activity and ATP content increased with +Epi. OS markers in proteins and lipids were reduced, while buffering systems (superoxide dismutase 2 and catalase protein and activities) increased. In white blood cells, we documented serial reductions in mitochondrial DNA content and citrate synthase activity with aging, which were either fully or partially reversed with +Epi. Results demonstrate that +Epi treatment yields positive effects on mitochondrial biogenesis and function, leading to decreased OS and improved SkM bioenergetics in aged rats.

Deer antler velvet (Cervus elaphus L.) is a traditional material in oriental medicine, extensively utilized for its anti-aging, antioxidant, and immune-boosting properties. Our prior research revealed that enzyme-derived deer antler velvet extract (YC-1101) stimulated the immune system by activating macrophages and augmenting splenocyte proliferation. In this study, we investigated the effect of YC-1101 on the proliferation, activation, and cytotoxicity of natural killer (NK) cells, emphasizing activation-receptor upregulation, cytokine secretion, and antitumor efficacy. Our findings demonstrated that YC-1101 treatment markedly enhanced NK cell proliferation in a dose-dependent and time-dependent manner by preserving mitochondrial function. NK cells expanded through YC-1101 treatment exhibited a significant increase in surface expression of activating NK receptors, NKG2D, and NKp44. Additionally, levels of immune-related cytokines like tumor necrosis factor-alpha, interferon-gamma, and granulocyte-macrophage colony-stimulating factor were substantially elevated in the YC-1101-treated group compared with control. Notably, NK cell activation induced by YC-1101 intensified cytotoxicity against various cancer cell lines, and combining YC-1101 with immune checkpoint inhibition synergistically enhanced antitumor activity. Collectively, our results indicate that integration of YC-1101 with expanded NK cells could be a promising approach to augment cancer treatment efficacy.

This study aimed to evaluate the protective effects of black raspberry (Rubus occidentalis L. L.), shady Jerusalem sage (Phlomis umbrosa Turcz.), and their combination (BLB301) on dexamethasone-induced muscle atrophy using both cellular and animal models. In the former, the cytotoxicity and mRNA expression of key anabolic and catabolic markers were evaluated in C2C12 cells subjected to hydrogen peroxide (H₂O₂)-induced oxidative stress and treated with the extracts. In the latter, male ICR mice were assigned to the following groups: control (CON), dexamethasone injection (DEX), and DEX receiving 100 mg/kg, 200 mg/kg, or 400 mg/kg BLB301. C2C12 cells treated with BLB301 exhibited higher scavenging activity and mTOR expression than the CON and DEX cells. The mice in the DEX group exhibited significantly lower body weight (b.w.), grip strength, and muscle-to-b.w. ratios and higher oxidative stress and catabolic marker (myostatin, atrogin-1, and MuRF1) expression levels than those in the other groups. BLB301 mitigated the foregoing effects in a dose-dependent manner by increasing the antioxidant enzyme activity and decreasing the malondialdehyde levels. It also upregulated key anabolic pathways (PI3K/Akt/mTOR/S6K1) and muscle-specific transcription factors (Myf5, MyoD, and myogenin). BLB301 also downregulated the catabolic markers and restored the balance between protein synthesis and degradation. Therefore, BLB301 alleviates dexamethasone-induced muscle atrophy by modulating oxidative stress and by promoting and inhibiting anabolic and catabolic pathways, respectively. The findings of this study demonstrate the potential of BLB301 as a therapeutic agent for muscle-wasting conditions.

Coumarins are a group of naturally occurring phytochemicals found in various plants with many bioactivities. Recently, it was reported that esculetin (6,7-dihydroxycoumarin) reduced food preference behavior of Caenorhabditis elegans dependent on the human µ-opioid receptor (MOPR). Thus, this study investigated the structure-activity relationships (SAR) of 17 coumarin analogs using a food preference assay in C. elegans. While the parent compound, coumarin, and single substitutions at C3, C5, C7, or C8 had no effect, modifications at C4 and C6 were critical for modulating this behavior. Specifically, 4-hydroxycoumarin, 4-methylcoumarin, 6-hydroxycoumarin, 4-hydroxy-6-methylcoumarin, 6,7-dihydroxycoumarin (esculetin), 7-hydroxy-6-methoxycoumarin (scopoletin), and several di-substituted derivatives significantly reduced the preference index, which was abolished in npr-17 (opioid receptor homolog) knockout strains. Additional determination of preference behaviors was conducted with a strain carrying the human MOPR, which showed results comparable to the wildtype, except for 4-hydroxy-6-methylcoumarin and scopoletin. This work demonstrates the potential antagonistic effects of selected coumarins and the utility of C. elegans as an in vivo model for SAR studies targeting human MOPR.

Hibiscus acid has antimicrobial activity against pathogenic bacteria; however, the mechanism of action against these bacteria has not been completely identified. The effect of hibiscus acid on the viability, motility, and cell membrane of multidrug-resistant enterohemorrhagic Escherichia coli, Salmonella Typhimurium, and Listeria monocytogenes was determined. Cell viability was determined by the pour plate technique, and motility was determined by phase contrast microscopy. Acridine orange/ethidium bromide fluorescent staining was performed using a fluorescence microscope to observe live and dead cells. Bacterial cell damage was analyzed by scanning electron microscopy. Finally, nucleotide leakage (DNA and RNA) was evaluated by measuring absorbance at 260 nm using a UV-VIS spectrophotometer. Hibiscus acid treatments (minimum inhibitory concentration [MIC], minimum bactericidal concentration [MBC], 10× minimum inhibitory concentration [10× MIC]) significantly decreased the viable cell counts of the three pathogenic bacterial strains in a time-dependent manner. Hibiscus acid at concentrations of MIC, MBC, and 10× MIC inhibited the motility of bacteria and caused lysis of the bacterial cell membrane. The damage to the membrane was greater as the concentration of hibiscus acid increased. High red fluorescence was found in the cells treated with hibiscus acid at the MIC and 10× MIC, and the release of intracellular material was observed after 2 h of treatment with the three pathogenic bacteria studied. The antimicrobial effect of hibiscus acid was due to the alteration of the membrane permeability of the three pathogenic bacteria studied. Hibiscus acid may represent an alternative to antibiotics for the treatment or prevention of infectious bacterial diseases.

Dietary modifications are recommended for individuals with hypercholesterolemia to reduce cardiovascular disease (CVD) risk. While almonds have been shown to improve certain CVD risk factors, the effects of almonds on high-density lipoprotein cholesterol (HDL-C) are less clear. This study aimed to determine the quantity of almonds that would provide optimal increases in HDL-C in a population with hypercholesterolemia. Participants were randomized (n = 25/group) to low-dose almond (LDA; 1.5 oz/day), high-dose almond (HDA; 2.5 oz/day), or nut-free diet (NFD; cookies isocaloric to LDA) for 16 weeks. Change in HDL-C (primary outcome), Framingham Risk Score (FRS), blood pressure (BP), apolipoproteins, anthropometrics, and serum α-tocopherol were assessed at baseline and weeks 4, 8, 12, and 16. There were no significant differences in HDL-C between groups; however, there were reductions in FRS of 1.4% and 0.6% from baseline at week 16 in the HDA and LDA groups (P ≤ .05), respectively, while the NFD group had a 1.0% decrease (P = .14). There were decreases of 4.7 mmHg, 4.1 mmHg, 5.1 mmHg, and 3.8 mmHg in systolic BP for the HDA group after 4, 8, 12, and 16 weeks, respectively (P ≤ .06), which was significantly lower than the NFD group from baseline at week 8. The NFD group had increases in sagittal abdominal diameter of 4.0% and 2.7% after 4 and 8 weeks (P ≤ .05), respectively, whereas the almond groups did not. Findings suggest almond consumption may support dietary strategies for improving CVD risk factors in adults with hypercholesterolemia.

Alcoholic liver injury (ALI) is a prevalent and severe form of liver disease that lacks specific therapies, relying instead on supportive care. In ALI, gut epithelial tight junction proteins are compromised, leading to increased intestinal permeability and the translocation of endotoxins, such as lipopolysaccharides (LPS), into the bloodstream, thereby aggravating liver injury. The plant Sicyos angulatus (SA), part of the Cucurbitaceae family, is recognized for its anti-inflammatory and antioxidant effects but has not yet been studied for potential efficacy in mitigating ALI. In this study, we induced ALI in mice by administering high oral doses of ethanol following pretreatment with or without SA. The SA-treated mice exhibited significantly lower levels of plasma alanine aminotransferase and aspartate aminotransferase, markers indicative of reduced liver damage. Despite observing no notable changes in hepatic fat accumulation or expression of alcohol metabolism-related genes, we found that the SA group exhibited a marked reduction in terminal transferase dUTP nick end labeling-positive hepatocytes and reactive oxygen species within the mitochondrial fraction of liver tissue. Additionally, SA preserved intestinal barrier integrity by upregulating genes associated with tight junctions in the ileum and colon, resulting in lower LPS levels in the blood. Complementary in vitro studies with Caco-2 cells further showed that SA pretreatment protected against LPS-induced tight junction disruption by inhibiting NF-κB pathway activation. Collectively, our findings indicate that SA protects against ALI by supporting gut barrier integrity, thereby limiting LPS translocation and hepatic oxidative stress. This study underscores the potential of SA as a therapeutic agent targeting the gut-liver axis.

Hair loss is characterized by reduced hair thickness, decreased density, and delayed growth and is associated with factors such as aging, stress, and environmental influences. This study investigated the effects of Gly-Pro-Val-Gly-Pro-Ser low molecular weight fish collagen peptide (FC) on improving hair health and alleviating hair loss. Human dermal papilla cells and C57BL/6 mice were used as experimental models. Mice were administered FC at doses of 200, 400, and 800 mg/kg body weight, followed by protein and RNA analyses and histological evaluations. The results showed that FC significantly increased the expression of vascular endothelial growth factor, PCNA, Hepatocyte growth factor, endothelial growth factor, and insulin-like growth factor 1, which play essential roles in hair follicle growth and regeneration. Additionally, FC administration reduced the expression of specific proteins negatively associated with hair health. Histological and morphological analyses revealed that FC enhanced hair follicle size, density, and overall hair quality. These findings suggest that FC may promote hair growth and regeneration.

EstroG-100®, a functional ingredient blend that has been used for menopausal health in women. However, detailed studies on its effects and their underlying mechanisms have been lacking. Herein, we evaluated the antifatigue effects of EstroG-100 using C2C12 cells exposed to oxidative stress and mice subjected to a forced swimming test. EstroG-100 significantly increased the viability and adenosine triphosphate (ATP) content of C2C12 cells under oxidative stress, while notably inhibiting the generation of reactive oxygen species. EstroG-100 tended to prolong the forced swimming time in mice. It also significantly inhibited the serum lactate dehydrogenase activity, increased intramuscular glycogen content, and upregulated the expression of peroxisme proliferator-activated receptor (PPAR)-δ and uncoupling protein (UCP)3 genes involved in β-oxidation of fatty acids. Furthermore, EstroG-100 significantly increased the activities of antioxidant enzymes, including catalase, superoxide dismutase, glutathione S-transferase, and glutathione levels, and decreased the malondialdehyde levels in the liver. These results indicate that EstroG-100 may contribute to recovery from physical fatigue by enhancing the antioxidant activity to alleviate oxidative stress and improving muscle function via modulation of glycogen and fatty acid metabolism.

Nonalcoholic fatty liver disease (NAFLD) is a global health issue, often associated with gut dysbiosis. In recent years, probiotics have gained attention as potential therapeutic agents for NAFLD. This study explored the effects of a single strain, Bacillus subtilis with high surfactin secretion, on C57BL/6 mice fed a high-fat diet (HFD), a model for NAFLD, for 13 weeks. We conducted efficacy assays over 13 weeks on liver fat accumulation and gut microbiome modulation. Bacillus supplementation reduced body weight gain and fat accumulation in the liver, but not in adipose tissues. This indicates a decoupling of hepatic and adipose lipid accumulation-meaning that lipid reduction occurred selectively in the liver, independent of changes in peripheral fat storage. Hepatic steatosis and liver enzyme levels were significantly improved. The supplementation largely maintained or amplified the bacterial abundance shifts caused by the HFD. Only seven-including Lactobacillus, Akkermansia, and Romboutsia-out of 53 bacterial genera which were significantly changed by HFD were restored to normal levels by the supplementation. These three genera are commonly regarded as beneficial for human health due to their roles in gut barrier integrity, immune modulation, and metabolic regulation. In contrast, despite these limited changes in bacterial composition, bacterial enzyme analysis suggested significant metabolic modulation by Bacillus supplementation. A single strain of Bacillus subtilis, instead of a mixture of multiple bacterial strains, can prevent hepatic steatosis without affecting fat tissue weight, underscoring its potential as a targeted therapeutic option through microbiome modulation of a few beneficial bacteria.