Triticale malt is an underutilized cereal matrix with high amylolytic potential, which may be exploited for the recovery of plant‐derived enzymes for food and biotechnological applications. This study aimed to obtain α‐amylase‐ and β‐amylase‐enriched aqueous extracts from Bicentenario and Siglo XXI triticale malts and to partially purify these enzymes using ethanol/trisodium citrate aqueous two‐phase systems (ATPS). Triticale grains were malted by germination for 5 days and dried at 50°C. Aqueous extraction was performed using ground malt and deionized water at a 1:10 ratio under different extraction times (30, 120, and 270 min) and temperatures (30°C and 40°C). The selected extracts were lyophilized and subjected to ATPS composed of ethanol and trisodium citrate. Enzyme activity was determined using the BETAMYL‐3 method for β‐amylase and the AOAC 2002.01, AACC 22‐02.01, and ICC Standard No. 303 methods for α‐amylase. Mild extraction conditions favored enzyme recovery, with the highest α‐amylase activity observed in Siglo XXI extract at 30 min/30°C, increasing from 99.10 CU/g in malt to 507.42 CU/g in the aqueous extract. β‐Amylase activity was also higher in Siglo XXI than in Bicentenario extracts. The 30% ethanol/18% trisodium citrate ATPS was the most effective system, promoting differential partitioning with α‐amylase concentrated in the bottom phase (432.89 CU/mL) and β‐amylase in the top phase (5.78 BU/mL). These results highlight the potential of triticale malt as a renewable source of amylolytic enzymes and support ethanol/trisodium citrate ATPS as a mild, sustainable strategy for obtaining amylase‐enriched fractions, although further optimization is needed to improve β‐amylase recovery and scalability.
Ampelopsis grossedentata , a traditional food–medicinal vine rich in flavonoids, was investigated here for its antiaging potential and underlying mechanisms. An ethanol extract (AGE) was chemically profiled by UHPLC–ESI–HRMS/MS (16 compounds identified; dihydromyricetin ≈192.7 mg g −1 ) and shown to contain high levels of phenolics and flavonoids (TPC 348.4 mg GAE·g −1 ; TFC 213.4 mg RE·g −1 ) with potent in vitro antioxidant activity (DPPH IC 50 34.3 ± 1.8 μg mL −1 ; ABTS IC 50 40.3 ± 4.8 μg mL −1 ). AGE protected SH‐SY5Y cells from H 2 O 2 ‐induced injury by reducing intracellular ROS, preserving viability, and decreasing apoptosis. In a D‐galactose–induced mouse aging model, oral AGE ameliorated behavioral and hippocampal histopathological changes, restored organ indices, increased serum antioxidant defenses (T‐AOC, SOD, CAT, and GSH‐Px), and reduced lipid peroxidation (MDA). Mechanistically, AGE upregulated Nrf2 and downstream effectors NQO1 and HO‐1 and reversed proapoptotic and proinflammatory gene changes (improved Bcl‐2/Bax ratio; decreased caspase‐3, p53, p65, and iNOS). Molecular docking supported potential interactions between AGE flavonoids and key antioxidant/antiapoptotic targets. Collectively, these findings indicate that AGE attenuates oxidative stress, inflammation, and apoptosis via activation of Nrf2 signaling and related pathways, supporting its promise as a food‐based candidate for prevention or mitigation of age‐related oxidative damage.
Background Metabolic dysfunction–associated steatotic liver disease (MASLD) is a highly prevalent chronic liver disorder for which effective pharmacological interventions remain limited, particularly at early stages. Geniposide (GP), a major bioactive component derived from the fruit of Gardenia jasminoides , has been reported to exert hepatoprotective, anti‐inflammatory, and antioxidant effects; however, its molecular mechanisms in MASLD have not been fully elucidated. Methods An MASLD mouse model was established by feeding ApoE knockout mice a high‐fat diet (HFD), followed by GP treatment for 8 weeks. Hepatic steatosis, lipid metabolism, oxidative stress, and inflammatory responses were evaluated using biochemical assays, histopathological analysis, and immunofluorescence. Unbiased Astral data‐independent acquisition (Astral‐DIA) proteomics was performed to identify differentially expressed proteins and enriched signaling pathways. In vitro validation was conducted using palmitic acid (PA)–treated THLE‐2 human hepatocytes. Results GP treatment significantly alleviated hepatic steatosis and lipid metabolic disorder in HFD‐fed mice. Compared with the HFD group, GP reduced serum TG levels from 1.38 ± 0.15 to 0.79 ± 0.10 mM ( p < 0.05) and hepatic TG content from 3.15 ± 0.47 to 2.21 ± 0.28 mmol/g protein ( p < 0.05). Proteomic analysis identified more than 7600 proteins and revealed CYP4A family members as prominent GP‐responsive proteins, with Cyp4a10 and Cyp4a14 reduced by approximately 62% and 71%, respectively. Consistently, GP decreased hepatic 20‐HETE levels from 114.6 ± 28.52 to 80.63 ± 19.12 ng/mg protein ( p < 0.05) and reduced oxidative and inflammatory responses, including decreased serum IL‐6 from 127.3 ± 42.27 to 77.67 ± 23.55 pg/mL and TNF‐α from 44.18 ± 10.47 to 28.58 ± 8.53 pg/mL (both p < 0.05). In vitro, GP restored PA‐reduced THLE‐2 cell viability from 69.0 ± 7.0% to 88.0 ± 8.0% of the control level ( p < 0.05) and decreased intracellular 20‐HETE levels from 60.77 ± 9.06 to 40.28 ± 7.82 ng/mg protein ( p < 0.05). GP also attenuated PA‐induced lipid accumulation, ROS generation, inflammatory cytokine secretion, and apoptosis. Pharmacological inhibition of 20‐HETE synthesis partially recapitulated these protective effects, supporting the involvement of the CYP4A/20‐HETE axis in hepatocyte lipotoxicity. Conclusions GP ameliorates MASLD by attenuating hepatocyte lipotoxic injury through coordinated suppression of the CYP4A/20‐HETE axis and downstream ROS/NF‐κB‐mediated oxidative and inflammatory signaling. These findings provide mechanistic insight into the hepatoprotective actions of GP and highlight CYP4A‐associated lipid signaling as a therapeutically relevant pathway for the prevention and early intervention of MASLD.
This study investigated the phytochemical composition, antioxidant capacity, and anti‐inflammatory potential of ethanolic leaf extracts of Piliostigma malabaricum and Cheniella lakhonensis . Preliminary phytochemical screening showed that both species contained phenolic compounds, flavonoids, tannins, saponins, and cardiac glycosides, indicating diverse secondary metabolites. Quantitative analysis showed that C. lakhonensis contained higher total phenolic, flavonoid, and tannin contents than P. malabaricum . The antioxidant activity of the extracts was assessed using the DPPH radical‐scavenging assay and was significantly stronger in C. lakhonensis (IC 50 = 132.77 ± 3.80 μg/mL) than in P. malabaricum (IC 50 = 322.96 ± 2.77 μg/mL), compared with ascorbic acid (IC 50 = 68.25 ± 2.30 μg/mL). Both extracts demonstrated significant suppression of albumin denaturation under the evaluated in vitro conditions, indicating initial anti‐inflammatory capabilities, with P. malabaricum showing a slightly higher inhibitory effect. HPLC quantification and LC‐MS analysis investigations verified the existence of quercetin and quercitrin in both species, with elevated concentrations observed in C . lakhonensis . These results offer initial in vitro evidence suggesting that both species could be valuable sources of bioactive compounds; nonetheless, further antioxidant assays, mechanistic research, safety assessments, and in vivo studies are necessary prior to confirming their functional food or therapeutic uses.
The biological relevance of milk‐derived bioactive peptides depends not only on their reported bioactivities but also on whether they remain biologically relevant following intestinal epithelial exposure. Here, we used an integrated multiplatform workflow to determine whether combining epithelial metabolomic profiling, immunomodulatory screening, and epithelial handling could improve the assessment of the biological relevance of casein‐derived peptides. Four bovine casein–derived peptides, FVAPFPEVFG, NLLRF, EMPFPKY, and SDIPNPIGSENSEK, were evaluated using Caco‐2 LC‐MS/MS metabolomic profiling and RAW 264.7 immunomodulatory screening, both performed in technical duplicate ( n = 2), together with Caco‐2 epithelial handling studies. Untargeted LC‐MS/MS metabolomics identified 251 differential intracellular positive‐ion features, 341 extracellular positive‐ion features, and 48 intracellular negative‐ion features, demonstrating extensive peptide‐associated metabolic remodeling. Peptide exposure was associated with remodeling of both intracellular and extracellular metabolic pathways, with the most consistent changes centered on arginine‐related amino acid metabolism and linked central carbon metabolism. Although the four peptides produced distinct metabolic fingerprints, they converged on related epithelial metabolic nodes. In LPS‐stimulated RAW 264.7 macrophages, the peptides showed sequence‐dependent immunomodulatory activity: FVAPFPEVFG produced the strongest broad suppression of inflammatory mediators, EMPFPKY showed a selective immunomodulatory profile, SDIPNPIGSENSEK showed preliminary activity in a single‐point screen, and NLLRF showed no detectable immunomodulatory activity under the tested conditions. To determine whether a multifunctional peptide remained biologically relevant following epithelial exposure, EMPFPKY was selected for Caco‐2 transport studies. LC‐MS/MS reproducibly detected the EMPFPK and EMPFP peptide fragments during transepithelial passage, while live‐cell fluorescence imaging supported cell‐associated uptake of peptide‐derived material. Integrating epithelial metabolomics, immunomodulatory screening, and epithelial handling strengthens the assessment of the potential biological relevance of milk‐derived bioactive peptides beyond conventional bioactivity screening. Although these findings provide mechanistic insight, they are based on complementary in vitro epithelial and macrophage models and require validation in more physiologically relevant systems.
The quality of sauerkraut is determined by the combined effects of plant matrix, salinity, and starter culture ecology. However, there is limited literature on how kombucha‐assisted fermentation modulates these responses in white and purple cabbage systems. This study evaluated the interactive effects of cabbage matrix, brine NaCl concentration, and kombucha starter culture on fermentation performance, culturable microbial dynamics, safety‐related chemistry, antioxidant‐related responses, and descriptive sensory quality. White and purple sauerkraut samples were generated using a three‐factor full factorial design incorporating three salt concentrations (2.5%, 5.0%, and 7.5%, w/v) and two fermentation strategies (spontaneous and kombucha‐assisted fermentation). Fermentations were performed at 25°C ± 0.5°C for 28 days. Across all treatments, pH ranged from 2.83 to 5.42, titratable acidity ranged from 0.09% to 2.34% as lactic acid, and salt content ranged from 2.11% to 13.81%, confirming a treatment‐dependent acidification trend. At 28 days, reducing sugar, soluble protein, and nitrite levels ranged from 0.3940 to 0.9250 mg/100 mg, 0.6533 to 3.3700 mg/100 g, and 5.9433 to 13.2433 mg/kg, respectively. Total phenolic content, ascorbic acid, and DPPH IC 50 values ranged from 39.9067 to 84.5733 mg GAE/100 g, 128.6170 to 156.3170 mg/100 g, and 26.1800 to 46.8367 ppm, respectively. Moderate salinity, particularly 5.0% NaCl, resulted in the most consistent process yield, supporting acidification, microbial control, nitrite reduction, antioxidant‐related performance, and sensory integration. Kombucha‐assisted applications improved the selected response patterns, especially under moderate salinity, but the effect was largely matrix‐dependent. The findings suggest that kombucha‐assisted sauerkraut should be interpreted not as a simple inoculated product but as an interaction‐oriented fermentation system.
Lophopetalum wightianum Arn. has previously been identified as a medicinal plant reported to contain promising anti‐inflammatory and anticancer compounds, including lupeol and pristimerin. Compared to other species of the Lophopetalum genus, L. wightianum remains largely unstudied, and this study aimed to assess the analgesic, anti‐inflammatory, antipyretic, and antioxidant potential of the methanolic extract of its leaves and undertake a phytochemical investigation. Gas chromatography–mass spectrometry (GC–MS) analysis of the crude extracts indicated the presence of steroids, triterpenoids, and fatty acid esters. Lupeol, a triterpenoid, was isolated from the hexane fraction of the bark. In the writhing test of analgesic potential, 400 and 500 mg/kg dose groups of the leaf extract showed reduced mean writhing counts of 35.60 ± 0.87 ( p < 0.01) and 27.20 ± 1.59 ( p < 0.001), respectively, compared to the control group (42.20 ± 1.16). At the 500 mg/kg dose, the extract reduced licking duration by 40.09 ± 0.02% in phase one and 44.66 ± 0.01% in phase two of the licking test. Significant protection level (38.21 ± 1.56%, p < 0.001) was observed in the hotplate test at a dose of 500 mg/kg at 0.5 h, which was close to diclofenac sodium (40.70 ± 1.10%). A dose‐dependent effect was evident in the writhing, licking, and hotplate tests. In the anti‐inflammatory test, the highest anti‐inflammatory effect (36.79 ± 0.01%) was observed at 3 h at the highest dose, and a dose‐dependent effect was apparent. Finally, in the antipyretic activity test, the crude extract was most effective at a dose of 500 mg/kg. Overall, the findings indicate the presence of potential therapeutic bioactive compounds in the plant.
Objective The mechanism by which bovine colostrum secretory immunoglobulin A (SIgA) prevents alcoholic liver injury, particularly whether it acts through the nuclear factor E2‐related factor 2 (Nrf2) pathway in a dose‐dependent manner, remains unclear. This study investigated the preventive effects of SIgA against acute alcoholic liver injury in mice and tested the hypothesis that SIgA activates the Keap1/Nrf2/HO‐1 (heme oxygenase‐1) pathway in a dose‐dependent manner, with optimal protection achieved at an intermediate dose via maximal hepatic accumulation. Methods Mice were pretreated with SIgA (20, 40, 80 mg/kg) for 28 days before ethanol challenge. Serum biochemistry, hepatic antioxidant enzymes, inflammatory cytokines, histopathology, and ultrastructure were assessed. Hepatic SIgA content was measured by ELISA. Keap1, Nrf2, and HO‐1 mRNA were detected by RT‐PCR. The Nrf2 inhibitor ML385 was used to verify pathway dependence. Results SIgA pretreatment significantly reduced serum transaminases, triglycerides, and hepatic malondialdehyde, while enhancing superoxide dismutase, glutathione, and catalase and suppressing tumor necrosis factor‐α and interleukin‐6. Protective effects showed a bell‐shaped dose–response, with the medium dose (40 mg/kg) being most effective. Hepatic SIgA content correlated strongly with Nrf2 and HO‐1 expression. ML385 coadministration reversed SIgA‐induced Keap1 downregulation and Nrf2/HO‐1 upregulation, confirming Nrf2/ARE (antioxidant response element) pathway dependence. Conclusion Bovine colostrum SIgA exerts dose‐dependent protection against acute alcoholic liver injury. The optimal effect at the medium dose is attributable to maximal hepatic SIgA accumulation, driving robust activation of the Keap1/Nrf2/HO‐1 pathway.
Background Diabetes mellitus is a severe metabolic disease in the world, and therefore significant research has been conducted on food‐derived bioactive compounds capable of antidiabetic effects. The Azadirachta indica (neem) plant, which is widely used in traditional food and ethnomedicine, contains a variety of phytochemicals that have potential applications in nutrition as nutraceuticals. Aims This meta‐analysis and systematic review assessed the antidiabetic effects of A. indica preparations in rodents with diabetes and more so in relevancy in terms of translation to food biochemistry, nutraceutical formulation and molecular nutrition pathway. Methods In accordance with PRISMA 2020, we performed a systematic search of PubMed, Scopus, Web of Science and Google Scholar to identify controlled studies on antidiabetic effects of A. indica on rodent diabetes models. The SYRCLE tool was used to determine the risk of bias. Primary outcome: improvement of fasting blood glucose (FBG). Secondary outcomes: glycated haemoglobin (HbA1c), insulin, oxidative stress biomarkers (SOD, catalase, GSH, GPx, MDA) and lipid profile parameters. Random‐effects meta‐analyses estimated the standardized mean differences (SMDs) using the g correction of Hedges. Duration, dose, extract type and diabetes induction method were analysed as subgroups. The I 2 statistics and tau‐squared ( τ 2 ) were used to measure heterogeneity. Results The meta‐analysis comprised the studies that were conducted on the different A. indica preparations in the diabetic rats. A. indica had a significant effect of reducing FBG with a pooled effect size of −6.702 (95% CI: −7.621–5.165, p = 0.001), but with high heterogeneity ( I 2 = 92.6). A. indica had a significant pooled effect of improving oxidative stress markers, improving SOD activity (SMD = 2.222, 95% CI: 0.999 to 3.450), favourable lipid profile changes included reduced total cholesterol (SMD = −3.632, 95% CI: −4.814 to −2.450), triglycerides (SMD = −4.842, 95% CI: −6.206 to −3.477), LDL cholesterol (SMD = −3.471, 95% CI: −4.701 to −2.241) and increased HDL cholesterol (SMD = 3.280, 95% CI: 2.112 to 4.447). Conclusion A. indica exhibits strong nutraceutical potential for diabetes management through its multitarget actions on glycaemic control, enhancement of antioxidant defence and regulation of lipid metabolism. These effects are largely attributed to key bioactive constituents, including quercetin, nimbin and azadirachtolide, which appear to act through pathways involving AMPK activation, GLUT4 translocation and PPARγ modulation. Together, these findings provide solid preclinical support for the development of A. indica as a functional food ingredient or complementary dietary supplement aimed at improving metabolic health.
Opuntia ficus-indica peel is known to possess antioxidant, anti-inflammatory, and anticancer activities and currently is discarded or used for animal feeding. Within this context, the aim of this work was to evaluate the antiproliferative and pro-apoptotic effect of purple prickly pear peel extract (PPE) on the human colon adenocarcinoma cancer cell line (HTC116). The methanolic extract of PPE was characterized in terms of betalain and polyphenols as well as total antioxidant capacity. Cell viability, apoptosis induction, cell cycle arrest, and reactive oxygen species (ROS) production assays were performed. Important proteins and genes related to proliferation and apoptosis were determined. PPE represents a good source of bioactive compounds with a high antioxidant capacity. Cell viability was reduced gradually by PPE treatments, with lower effects in nontumorigenic cells. Compared to the control group, a significant induction of apoptosis as well as cell cycle arrest in the sub-G1 phase and ROS production was observed in PPE-treated cells. Furthermore, the treatment induced the overexpression of p53 at protein levels and upregulated the mRNA expression of pro-apoptotic BAX, CASP9, BID, and CYCS, along with the significant decrease of anti-apoptotic BCL2 gene expression. Simultaneously, cyclin D1 and CDK4 gene expression were significantly decreased, while p21 increased considerably. The treatment also induced the downregulation of Her2 and PI3K at protein levels and caused the suppression of PI3KCA and mTOR expression at gene levels. Overall, these findings suggested that PPE has potential anticancer effects against human colon adenocarcinoma progression.
Food-derived flavonoids are of increasing interest as bioactive compounds relevant to nutraceutical and functional-food research, but mutation-aware prioritization of such compounds remains limited in intrahepatic cholangiocarcinoma (CCA). Whole-exome sequencing data from seven tumor-normal matched CCA pairs were reanalyzed and integrated with mutation annotation, structural mapping, cell-based assays, molecular docking, and 100-ns molecular dynamics simulations. The cohort showed marked intertumoral heterogeneity, with 324-1244 nonsilent mutations per tumor. A recurrent cluster of EEF1A2 alterations was identified within codons 353-393, including codon 361 substitutions observed in three tumors. Because these codon 361 events involved adjacent nucleotides within the same codon and phasing information was unavailable in the public dataset, the pattern is interpreted conservatively as a candidate recurrent alteration cluster rather than a validated driver hotspot. In HuCCT-1 cells, the ectopic expression of EEF1A2-I361M or EEF1A2-I361L increased proliferation and wound closure relative to wild-type EEF1A2, with I361M showing a stronger phenotype. Structure-guided docking and molecular dynamics simulations further suggested predicted allele-dependent interaction profiles of luteolin, morin, and taxifolin near the mutated region. These computational results are presented as hypothesis-generating prioritization outputs and not as proof of direct target engagement or allele-selective biological activity. Overall, the findings identify EEF1A2 codon 361 as a candidate molecular context for future validation of food-derived flavonoids in CCA-related research.
The Sundarbans mangrove ecosystem represents a unique ecological niche enriched with diverse medicinal plant species exhibiting significant therapeutic potential. This review summarizes the hepatoprotective phytochemicals derived from mangrove plant species of the Sundarbans and highlights their pharmacological mechanisms. A comprehensive literature search up to 2024 was conducted using major scientific databases to identify studies reporting hepatoprotective phytochemicals from mangrove plant species. A total of 48 bioactive metabolites belonging to diverse chemical classes, including terpenoids, alkaloids, flavonoids, phenolics, quinones, polysaccharides, glycosides, lignans, peptides, and fatty acids, were identified from 15 mangrove species. These metabolites exhibit hepatoprotective effects by mitigating oxidative stress, inflammation, apoptosis, and fibrosis, which are key pathological processes involved in liver injury. Mechanistically, many metabolites regulate important molecular pathways such as nuclear factor kappa–light‐chain‐enhancer of activated B (NF‐κB), mitogen‐activated protein kinase (MAPK), and nuclear factor erythroid 2–related factor 2 (Nrf2), while also normalizing liver biomarkers including alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and gamma‐glutamyl transpeptidase (GGT). Overall, mangrove plant species of the Sundarbans represent a promising natural source of hepatoprotective agents.
The limited storability of hawthorn fruits is primarily due to rapid metabolic changes that compromise fruit quality. While cold storage is recommended to stall this process, it can induce chilling injury (CI) characterized by pitting. In this study, the impact of gamma-aminobutyric acid (GABA) (GABA-0, GABA-5 mM, and GABA-10 mM) on "Sultan" hawthorns stored at 2 degrees C and 90% RH for 120 days was evaluated. Both GABA treatments effectively reduced CI, maintaining fruit quality with greener peels, higher membrane stability index (MSI), and better retention of firmness and titratable acidity (TA), while reducing total soluble solids (TSS) compared to the control. GABA treatments reinforced the antioxidant defense system, increasing activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), as well as concentrations of total phenol content (TPC), total flavonoid content (TFC), and vitamin C. Treatment with GABA reduced the activities of hydrolytic enzymes and polyphenol oxidase (PPO), as well as microbial counts and decay incidence. The findings indicate that GABA at 10 mM reduced CI by 6% compared with the control (20% after 120 days of cold storage), while also contributing to delayed senescence and improved maintenance of quality attributes in hawthorn fruit.
The consumption of high-sugar diets by women of reproductive age can adversely affect reproductive health by inducing hormonal and metabolic imbalance. This study investigated the efficacy of a natural compound, ginsenoside Rg1, in mitigating these negative phenotypes. It was found that prolonged high-sugar intake led to obesity, lipid accumulation, ovarian atrophy, and reproductive disorders in female fruit flies. Treatment with ginsenoside Rg1 significantly alleviated the reproductive damage caused by the high-sugar diet, including observed increases of 59.49% in egg production, 84.48% in pupariation numbers, and 19.68% in pupation success. Ginsenoside Rg1 also prevented sugar/fat accumulation, stabilized insulin levels, elevated the concentrations of 20-hydroxyecdysone (20E), and restored endocrine balance. Mechanistically, Rg1 exhibited cellular target engagement with the insulin receptor (INR), leading to enhanced expression of its downstream extracellular signal-regulated kinase (ERK) and estrogen receptor (ER) and increased insulin signaling. Rg1 also showed cellular target engagement with the steroid hormone receptor (ecdysone receptor [ECR]), boosting ecdysone-induced protein 75B (Eip75B) and broad (Br) expression to activate steroid hormone signaling. These pathways acted synergistically to modulate expression of the yolk protein receptor and vitellogenin, critical for oogenesis. Molecular docking simulations predicted that Rg1 could interact with INR and ECR, a prediction corroborated by CETSA data indicating cellular target engagement. These findings collectively support a mechanistic model in which Rg1 physically engages both receptors to modulate downstream signaling. Alterations in gene expression in INR- and ECR-mutant flies confirmed the mutual influence of insulin and steroid hormone signaling. Ginsenoside Rg1 may thus activate both insulin- and steroid hormone-related signaling pathways to alleviate reproductive damage caused by high-sugar diets. Furthermore, the activation of steroid hormone signaling by Rg1 was dependent on the presence of insulin signals. These findings provide preliminary mechanistic insights and generate testable hypotheses for future investigation into the potential of Rg1 in addressing reproductive disorders associated with long-term excessive sugar intake.
Phenolic compounds, also known as (poly)phenols, are major phytochemicals characterized by diverse chemical structures. Prenylation, a hydrophobic modification, occurs naturally on various (poly)phenols. Prenylated derivatives of p-coumaric acid, such as drupanin and artepillin C, are characteristically found in Brazilian green propolis (BGP), which is derived from Baccharis dracunculifolia DC. (Asteraceae). However, studies on the bioavailability of prenylated derivatives of (poly)phenols remain limited. In this study, we investigated the intestinal absorption pathways of prenylated derivatives of p-coumaric acid present in BGP using thoracic lymph-cannulated rats. BGP was solubilized in 10% propylene glycol and administered in the stomach of fasting rats. Lymph and peripheral plasma samples were analyzed using liquid chromatography-tandem mass spectrometry. Both the intact compounds and their conjugated metabolites, including glucuronides and sulfates, were detected in the lymph and plasma. At a dose of 300 mg BGP/kg, the lymphatic/peripheral plasma ratios of p-coumaric acid and its monoprenylated form, drupanin, were 21% and 16%, respectively. These ratios increased following the administration of 30 mg/kg. Notably, artepillin C, a diprenylated derivative of p-coumaric acid, exhibited preferential lymphatic transport, with lymphatic/peripheral plasma ratio of 72% at 300 mg BGP/kg. At a 30 mg/kg dose, its concentration in the lymph was 10-fold higher than that in the plasma. The concentration ratios in the lymph and peripheral plasma were correlated to the octanol/water partition coefficients of these compounds, indicating that the addition of prenyl groups increased the hydrophobicity of these compounds and may facilitate their lymphatic transport. In conclusion, diprenylated derivative artepillin C was highly hydrophobic and transported to the lymphatic system after intestinal absorption. These results will contribute to elucidating the pharmacokinetic properties of prenylated derivatives of (poly)phenols.
Skeletal muscle insulin resistance is a key feature of Type 2 diabetes and is closely related to impaired glucose uptake. Inulin‐type fructans are commonly used as dietary fibers, but their direct effects on insulin‐responsive cells are not well defined. In the present study, the effect of chicory inulin on palmitate‐induced insulin resistance was examined in C2C12 myotubes. Chicory inulin was characterized before use. Palmitate treatment reduced glucose uptake and disrupted insulin signaling in C2C12 myotubes. Treatment with chicory inulin increased glucose uptake and promoted GLUT4 translocation. Inhibitory phosphorylation of IRS‐1 was also reduced. In addition, mitochondrial membrane potential and ATP levels were improved, while the production of inflammatory cytokines was decreased. The expression of SNX27 was increased in cells treated with chicory inulin. Overexpression of SNX27 showed similar effects on glucose uptake and insulin signaling. Silencing of SNX27 weakened these effects. Changes in PI3K/AKT and NF‐κB signaling were observed under the same conditions. Taken together, CI exposure was associated with improved insulin‐resistance‐related cellular responses in PA‐treated C2C12 myotubes. These effects may involve SNX27‐associated processes. These findings should be interpreted as exploratory cellular‐level evidence obtained under controlled in vitro conditions, rather than as direct evidence that intact dietary inulin reaches skeletal muscle or produces the same effects in vivo.
This study investigated the in vitro α‐glucosidase (α‐GLU) and dipeptidyl peptidase‐IV (DPP‐IV) inhibition by mung bean fractions and red kidney bean (RKB) and tested the effect of a mung bean coat (MBC)–enriched coffee blend on postprandial glucose and insulin responses in healthy individuals. The mung bean fraction, particularly its seed coat, showed significantly higher inhibition of α‐GLU (74.20%) and DPP‐IV (55.42%) than all tested RKB samples. Blends of MBC‐enriched coffee were formulated by combining roasted MBC with coffee powder at different ratios. The 75:25 blend exhibited the highest enzyme inhibition (27.10% α‐GLU and 68.93% DPP‐IV inhibition). A 50:50 blend was selected for clinical testing based on its sensory appeal. In the randomized crossover in vivo trial, MBC‐enriched coffee significantly reduced postprandial glucose levels by 6.5 and 5.5 mg/dL at 15 and 30 min and insulin levels by 30.78, 29.36, and 25.92 µIU/mL at 15, 30, and 60 min, respectively, compared to control coffee. These findings suggest that MBC could be an ingredient for managing blood glucose levels in functional products.
BackgroundUlcerative colitis (UC), an inflammatory bowel disease, presents a challenge due to the limited treatment options available. Increasing studies have indicated that colonic motor dysfunction is an effective strategy to mitigate the symptoms of UC. This study aimed to investigate the therapeutic effect of cardamonin (CAD) on acetic acid (AA)-induced UC in rats and to elucidate its underlying mechanisms in modulating colonic motility.MethodsA rat UC model was applied through rectal administration of AA. The therapeutic effects of CAD were evaluated using the disease activity index, colon weight/length ratio, and histopathological (Riley) scores. Colonic motility was assessed by measuring fecal water content and transit velocity. Antioxidant capacity was determined by measuring malondialdehyde (MDA) and superoxide dismutase (SOD) levels. Quantitative real-time PCR (qPCR) was used to analyze the gene expression of the acetylcholine (ACh)/nitric oxide (NO) interstitial cells of Cajal (ICC)-anoctamin 1 (ANO1) pathways, which critically modulates colonic motility. Additionally, in vitro organ bath experiments quantified smooth muscle responses to neurotransmission modulators.ResultsCAD effectively inhibited AA-induced UC in rats, as evidenced by the alleviation of the DAI score, ulcer index, macroscopical score, colon weight/length ratio, and Riley score, as well as reduced MDA levels and increased SOD activity in colon tissue. High-dose (120 mg/kg) and low-dose (60 mg/kg) CAD both exhibited significant interventional effects on UC rat models, and high-dose CAD produced a better interventional effect compared with low-dose CAD. Additionally, the AA-induced UC model demonstrated upregulated mRNA expression of acetylcholine esterase (AChE) and anoctamin 1 (ANO1) and downregulated mRNA expressions of c-kit and nitric oxide synthase (NOS1) in colonic tissue. Notably, pretreatment with CAD reversed these AA-induced alterations. Furthermore, the contractions of longitudinal smooth muscle induced by various substances that regulate neurotransmission-related contractions, including the ACh agonist carbachol, the ANO1 channel blocker 5-nitro-2-(3-phenylpropylamino) benzoic acid, and the NO inhibitor NG-nitro-L-arginine methyl ester hydrochloride, were inhibited by CAD.ConclusionWe showed for the first time the upregulation of the ACh-ICC-ANO1 pathway and the downregulation of the NO-ICC-ANO1 pathways in the AA-induced UC model. Moreover, we found that a novel perspective on the anticolitis potential of CAD through modulating the Ach/NO-ICC-ANO1 pathway in colonic neurotransmission.
Soy peptides (SPs) have been extensively studied with an emphasis on their immune‐boosting effects and production‐associated bitterness. This associated bitterness affects SPs’ oral consumption despite their bioactivities. In this review, the immune‐boosting functions, factors affecting bitterness, and consumers’ perceptions of SPs are explored. Debittering/masking strategies to improve SP acceptability for oral consumption and formulation of SP‐based food products are ultimately provided. It is established that SPs can contribute to immune functions despite different factors affecting bitterness perception by consumers, ranging from dietary and culinary to genetic and other components of the food matrix. Furthermore, SP bitterness levels can be reduced using a wide range of biophysicochemical debittering and masking methods. This review provides a unique and integrative perspective by linking the immune‐boosting functions of SPs directly to the critical challenge of bitterness and its mitigation. Future studies focusing on highly efficient debittering techniques that support the immune‐boosting effect, quality, and mouthfeel of SPs and SP‐incorporated products are warranted.
Green tea processed from etiolated leaves exhibits a distinctive umami taste and fresh aroma, however, the specific compositional changes in the fresh leaves of etiolated Zhonghuang No. 1 during green tea processing-particularly regarding mechanisms of glycolipid metabolism regulation-remain poorly understood. In this study, we began by quantifying the bioactive components of etiolated green tea and then analyzed metabolite dynamics and glycolipid-lowering potential during processing using untargeted metabolomics and in vitro enzyme inhibition assays, respectively. Our key findings indicate that curl-shaped tea (DT) underwent the most substantial metabolic shifts, characterized by marked alterations in sugar and linoleic acid metabolites, alongside rapid accumulation of amino acids, phenylpropanoids, and terpenoids. In contrast, during flower-shaped tea (ST) formation, flavonoids, phenylpropanoids, terpenoids, and amino acids exhibited marked compositional shifts. These results indicate that processing-driven accumulation of flavonoids and terpenoids underpins the hypoglycolipidemic effects, providing mechanistic insights for developing yellow leaf green tea (YLGT) as a functional food regulating glycolipid metabolism.
