RESUMEN

To improve the extraction process and quality of Camellia oleifera Abel. oil (COO). This study examined the influence of explosion-puffing (EP) pretreatment on the physicochemical properties, characteristic compounds and sensory quality of the COO. The results revealed that the seeds after EP pretreatment had cavities surface, which facilitated the extraction of the COO and the dissolution of bioactive compounds. Compared to the untreated group, the oil yield of the 6-7%/20 min was increased from 71.41 to 88.94%, as well as higher levels of squalene, phytosterol, α-tocopherol, and phenolic acids, leading to an increase in the antioxidant abilities. Moreover, the fatty acid composition in the COO was not significantly affected (P > 0.05). W1C, W5S, W3C, W5C, and W1W were the main sensors to distinguish the flavor profile of the COO. In summary, EP pretreatment may be a promising method for enhancing oil yield and quality of the COO.

Asunto(s)

Camellia , Aceites de Plantas , Semillas , Gusto , Camellia/química , Semillas/química , Aceites de Plantas/química , Antioxidantes/química , Humanos , Manipulación de Alimentos , Ácidos Grasos/química , Ácidos Grasos/análisis

RESUMEN

Bioactive peptides, derived from short protein fragments, are recognized for their neuroprotective properties and potential therapeutic applications in treating central nervous system (CNS) diseases. However, a significant challenge for these peptides is their ability to penetrate the blood-brain barrier (BBB). EVSGPGYSPN (EV-10) peptide, a walnut-derived peptide, has demonstrated promising neuroprotective effects in vivo. This study aimed to investigate the transportability of EV-10 across the BBB, explore its capacity to penetrate this barrier, and elucidate the regulatory mechanisms underlying peptide-induced cellular internalization and transport pathways within the BBB. The results indicated that at a concentration of 100 µM and osmotic time of 4 h, the apparent permeability coefficient of EV-10 was Papp = 8.52166 ± 0.58 × 10-6 cm/s. The penetration efficiency of EV-10 was influenced by time, concentration, and temperature. Utilizing Western blot analysis, immunofluorescence, and flow cytometry, in conjunction with the caveolin (Cav)-specific inhibitor M-ß-CD, we confirmed that EV-10 undergoes transcellular transport through a Cav-dependent endocytosis pathway. Notably, the tight junction proteins ZO-1, occludin, and claudin-5 were not disrupted by EV-10. Throughout its transport, EV-10 was localized within the mitochondria, Golgi apparatus, endoplasmic reticulum, lysosomes, endosomes, and cell membranes. Moreover, Cav-1 overexpression facilitated the release of EV-10 from lysosomes. Evidence of EV-10 accumulation was observed in mouse brains using brain slice scans. This study is the first to demonstrate that Cav-1 can facilitate the targeted delivery of walnut-derived peptide to the brain, laying a foundation for the development of functional foods aimed at CNS disease intervention.

Asunto(s)

Barrera Hematoencefálica , Juglans , Péptidos , Juglans/química , Juglans/metabolismo , Barrera Hematoencefálica/metabolismo , Animales , Ratones , Péptidos/química , Péptidos/metabolismo , Péptidos/farmacología , Transporte Biológico , Caveolinas/metabolismo , Caveolinas/química , Humanos , Endocitosis , Proteínas de Plantas/metabolismo , Proteínas de Plantas/química , Nueces/química , Nueces/metabolismo

RESUMEN

The term type 3 diabetes mellitus (T3DM) has been considered for Alzheimer's disease (AD) due to the common molecular and cellular characteristics found between type 2 diabetes mellitus (T2DM) and cognitive deficits. However, the specific mechanism of T3DM remains elusive, especially the neuroprotective effects of dietary components in hyperglycemic individuals. In this study, a peptide, Leu-Val-Arg-Leu (LVRL), found in walnuts significantly improved memory decline in streptozotocin (STZ)- and high-fat-diet (HFD)-stimulated T2DM mouse models (p < 0.05). The LVRL peptide also mitigated hyperglycemia, enhanced synaptic plasticity, and ameliorated mitochondrial dysfunction, as demonstrated by Morris water maze tests, immunoblotting, immunofluorescence, immunohistochemistry, transmission electron microscopy, and cellular staining. A Wnt3a inhibitor, DKK1, was subsequently used to verify the possible role of the Wnt3a/ß-Catenin/GSK-3ß pathway in glucose-induced insulin resistance in PC12 cells. In vitro LVRL treatment dramatically modulated the protein expression of p-Tau (Ser404), Synapsin-1, and PSD95, elevated the insulin level, increased glucose consumption, and relieved the mitochondrial membrane potential, and MitoSOX (p < 0.05). These data suggested that peptides like LVRL could modulate the relationship between brain insulin and altered cognition status via the Wnt3a/ß-Catenin/GSK-3ß pathway.

Asunto(s)

Diabetes Mellitus Tipo 2 , Glucógeno Sintasa Quinasa 3 beta , Juglans , Fármacos Neuroprotectores , Proteína Wnt3A , beta Catenina , Animales , Diabetes Mellitus Tipo 2/metabolismo , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Masculino , Glucógeno Sintasa Quinasa 3 beta/metabolismo , Glucógeno Sintasa Quinasa 3 beta/genética , Ratones , Fármacos Neuroprotectores/farmacología , Fármacos Neuroprotectores/administración & dosificación , Fármacos Neuroprotectores/química , beta Catenina/metabolismo , beta Catenina/genética , Humanos , Ratas , Juglans/química , Proteína Wnt3A/metabolismo , Proteína Wnt3A/genética , Hiperglucemia/tratamiento farmacológico , Hiperglucemia/metabolismo , Ratones Endogámicos C57BL , Péptidos/química , Péptidos/farmacología , Péptidos/administración & dosificación , Células PC12 , Transducción de Señal/efectos de los fármacos

RESUMEN

Microglia phagocytose synapses have an important effect on the pathogenesis of neurological disorders. Here, we investigated the neuroprotective effects of the walnut-derived peptide, TWLPLPR(TW-7), against LPS-induced cognitive deficits in mice and explored the underlying C1q-mediated microglia phagocytose synapses mechanisms in LPS-treated HT22 cells. The MWM showed that TW-7 improved the learning and memory capacity of the LPS-injured mice. Both transmission electron microscopy and immunofluorescence analysis illustrated that synaptic density and morphology were increased while associated with the decreased colocalized synapses with C1q. Immunohistochemistry and immunofluorescence demonstrated that TW-7 effectively reduced the microglia phagocytosis of synapses. Subsequently, overexpression of C1q gene plasmid was used to verify the contribution of the TW-7 via the classical complement pathway-regulated mitochondrial function-mediated microglia phagocytose synapses in LPS-treated HT22 cells. These data suggested that TW-7 improved the learning and memory capability of LPS-induced cognitively impaired mice through a mechanism associated with the classical complement pathway-mediated microglia phagocytose synapse.

RESUMEN

Hydrophilic and hydrophobic modified nanomicelles might be more conducive to passage of the gastrointestinal barrier than walnut peptide (WP). In this study, a novel double modified starch polymer, SB-CST-DCA, was synthesized by grafting sulfabetaine (SB) and deoxycholic acid (DCA) onto corn starch (CST) molecules through etherification and esterification. The modification mechanism was discussed to determine its chemical structure, morphological properties, and thermal stability. Peptide-loaded nanomicelles (SB-CST-DCA-WP) were prepared using WP as the core material. The encapsulation efficiency and peptide loading amount reached 76.90 ± 1.52% and 18.27 ± 0.53%, respectively, with good stability and pH-responsive release behavior observed to effectively control WP release and enhance its antioxidant activity. The composite exhibited safety, non-toxicity, and good blood compatibility at concentrations below 125 µg/mL. Duodenum was identified as the main absorption site with an absorption ratio of 41.16 ± 0.36%.

Asunto(s)

Preparaciones de Acción Retardada , Portadores de Fármacos , Juglans , Micelas , Péptidos , Almidón , Almidón/química , Juglans/química , Péptidos/química , Preparaciones de Acción Retardada/química , Portadores de Fármacos/química , Humanos , Nanopartículas/química , Interacciones Hidrofóbicas e Hidrofílicas , Composición de Medicamentos , Proteínas de Plantas/química , Animales

RESUMEN

The aim of this study is to validate the activity of hazelnut (Corylus avellana L.)-derived immunoactive peptides inhibiting the main protease (Mpro) of SARS-CoV-2 and further unveil their interaction mechanism using in vitro assays, molecular dynamics (MD) simulations, and binding free energy calculations. In general, the enzymatic hydrolysis components, especially molecular weight < 3 kDa, possess good immune activity as measured by the proliferation ability of mouse splenic lymphocytes and phagocytic activity of mouse peritoneal macrophages. Over 866 unique peptide sequences were isolated, purified, and then identified by nanohigh-performance liquid chromatography/tandem mass spectrometry (NANO-HPLC-MS/MS) from hazelnut protein hydrolysates, but Trp-Trp-Asn-Leu-Asn (WWNLN) and Trp-Ala-Val-Leu-Lys (WAVLK) in particular are found to increase the cell viability and phagocytic capacity of RAW264.7 macrophages as well as promote the secretion of the cytokines nitric oxide (NO), tumor necrosis factor-α (TNF-α), and interleukin-1ß (IL-1ß). Fluorescence resonance energy transfer assay elucidated that WWNLN and WAVLK exhibit excellent inhibitory potency against Mpro, with IC50 values of 6.695 and 16.750 µM, respectively. Classical all-atom MD simulations show that hydrogen bonds play a pivotal role in stabilizing the complex conformation and protein-peptide interaction. Molecular Mechanics/Generalized Born Surface Area (MM/GBSA) calculation indicates that WWNLN has a lower binding free energy with Mpro than WAVLK. Furthermore, adsorption, distribution, metabolism, excretion, and toxicity (ADMET) predictions illustrate favorable drug-likeness and pharmacokinetic properties of WWNLN compared to WAVLK. This study provides a new understanding of the immunomodulatory activity of hazelnut hydrolysates and sheds light on peptide inhibitors targeting Mpro.

Asunto(s)

Corylus , Péptidos , Animales , Ratones , Proteasas 3C de Coronavirus/química , Proteasas 3C de Coronavirus/antagonistas & inhibidores , Proteasas 3C de Coronavirus/metabolismo , Corylus/química , Macrófagos/efectos de los fármacos , Macrófagos/inmunología , Simulación de Dinámica Molecular , Péptidos/química , Péptidos/farmacología , Proteínas de Plantas/química , Proteínas de Plantas/farmacología , Proteínas de Plantas/inmunología , Inhibidores de Proteasas/farmacología , Inhibidores de Proteasas/química , Células RAW 264.7 , SARS-CoV-2/efectos de los fármacos , SARS-CoV-2/inmunología , SARS-CoV-2/química , Células Vero

RESUMEN

We investigated the protective effect of walnut peptides and YVPFPLP (YP-7) on scopolamine-induced memory impairment in mice and ß-amyloid (Aß)-induced excitotoxic injury in primary hippocampal neurons, respectively. Additionally, the protective mechanism of YP-7 on neuronal excitotoxicity was explored. Mouse behavioral and hippocampal slice morphology experiments indicate that YP-7 improves the learning and memory abilities of cognitively impaired mice and protects synaptic integrity. Immunofluorescence, western blotting, and electrophysiological experiments on primary hippocampal neurons indicate that YP-7 inhibits neuronal damage caused by excessive excitation of neurons induced by Aß. HT-22 cell treatment with peroxisome proliferator-activated receptor γ (PPARγ) activators and inhibitors showed that YP-7 activates PPARγ expression and maintains normal neuronal function by forming stable complexes with PPARγ to inhibit the extracellular regulated protein kinase pathway. Therefore, YP-7 can ameliorate glutamate-induced excitotoxicity and maintain neuronal signaling. This provides a theoretical basis for active peptides to ameliorate excitotoxicity and the development of functional foods.

Asunto(s)

Hipocampo , Juglans , Trastornos de la Memoria , Neuronas , Péptidos , Animales , Humanos , Masculino , Ratones , Péptidos beta-Amiloides/metabolismo , Modelos Animales de Enfermedad , Hipocampo/efectos de los fármacos , Hipocampo/metabolismo , Juglans/química , Memoria/efectos de los fármacos , Trastornos de la Memoria/tratamiento farmacológico , Trastornos de la Memoria/inducido químicamente , Trastornos de la Memoria/metabolismo , Neuronas/efectos de los fármacos , Neuronas/metabolismo , Péptidos/química , Péptidos/farmacología , Proteínas de Plantas/química , Proteínas de Plantas/farmacología , PPAR gamma/metabolismo , PPAR gamma/genética , Escopolamina

RESUMEN

Correction for 'Therapeutic effects of a walnut-derived peptide on NLRP3 inflammasome activation, synaptic plasticity, and cognitive dysfunction in T2DM mice' by Yanru Li et al., Food Funct., 2024, 15, 2295-2313, https://doi.org/10.1039/D3FO05076A.

RESUMEN

AIMS: Ethyl hexanoate, one of the key flavor compounds in strong-flavor Baijiu. To improve the content of ethyl hexanoate in strong-flavor Baijiu, a functional strain with high yield of ethyl hexanoate was screened and its ester-producing performance was studied. METHODS AND RESULTS: Upon identification, the strain was classified as Candida sp. and designated as ZY002. Under optimal fermentation conditions, the content of ethyl hexanoate synthesized by ZY002 can be as high as 170.56 mg L-1. A fermentation test was carried out using the ZY002 strain bioaugmented Daqu to verify the role of the strain applied to Baijiu brewing. It was found that strain ZY002 could not only improve the moisture and alcohol contents of fermented grains but also diminish the presence of reducing sugar and crude starch. Furthermore, it notably amplified the abundance of flavor compounds. CONCLUSION: In this study, Candida sp. ZY002 with a high yield of ethyl hexanoate provided high-quality strain resources for the actual industrial production of Baijiu.

Asunto(s)

Candida , Caproatos , Ésteres , Fermentación , Alimentos Fermentados , Caproatos/metabolismo , Ésteres/metabolismo , Ésteres/análisis , Alimentos Fermentados/microbiología , Alimentos Fermentados/análisis , Candida/metabolismo , Aromatizantes/metabolismo , Microbiología de Alimentos , Bebidas Alcohólicas/microbiología , Bebidas Alcohólicas/análisis

RESUMEN

Food-derived peptides with low molecular weight, high bioavailability, and good absorptivity have been exploited as angiotensin-converting enzyme (ACE) inhibitors. In the present study, in-vitro inhibition kinetics of peanut peptides, in silico screening, validation of ACE inhibitory activity, molecular dynamics (MD) simulations, and HUVEC cells were performed to systematically identify the inhibitory mechanism of ACE interacting with peanut peptides. The results indicate that FPHPP, FPHY, and FPHFD peptides have good thermal, pH, and digestive stability. MD trajectories elucidate the dynamic correlation between peptides and ACE and verify the specific binding interaction. Noteworthily, FPHPP is the best inhibitor with a strongest binding affinity and significantly increases NO, SOD production, and AT2R expression, and decreases ROS, MDA, ET-1 levels, ACE, and AT1R accumulation in Ang II-injury HUVEC cells.

Asunto(s)

Inhibidores de la Enzima Convertidora de Angiotensina , Arachis , Células Endoteliales de la Vena Umbilical Humana , Péptidos , Peptidil-Dipeptidasa A , Inhibidores de la Enzima Convertidora de Angiotensina/farmacología , Inhibidores de la Enzima Convertidora de Angiotensina/química , Inhibidores de la Enzima Convertidora de Angiotensina/metabolismo , Humanos , Peptidil-Dipeptidasa A/metabolismo , Peptidil-Dipeptidasa A/química , Arachis/química , Péptidos/química , Péptidos/metabolismo , Péptidos/farmacología , Simulación de Dinámica Molecular , Simulación por Computador , Cinética , Unión Proteica

RESUMEN

Walnut dreg (WD) active peptides are an important source of dietary antioxidants; however, the products of conventional hydrolysis have limited industrial output owing to poor flavour and low bioactivity. To this end, in this study, we aimed to employ bvLAP, an aminopeptidase previously identified in our research, as well as commercially available Alcalase for bi-enzyme digestion. The flavour, antioxidant activity, and structures of products resulting from various digestion methods were compared. The results showed that the bi-enzyme digestion products had enhanced antioxidant activity, increased ß-sheet content, and reduced bitterness intensity from 9.65 to 6.93. Moreover, bi-enzyme hydrolysates showed a more diverse amino acid composition containing 1640 peptides with distinct sequences. These results demonstrate that bi-enzyme hydrolysis could be a potential process for converting WD into functional food ingredients. Additionally, our results provide new concepts that can be applied in waste processing and high-value utilisation of WD.

Asunto(s)

Antioxidantes , Juglans , Hidrólisis , Antioxidantes/química , Juglans/metabolismo , Hidrolisados de Proteína/química , Péptidos/química , Subtilisinas/metabolismo

RESUMEN

NLRP3 inflammasome activation plays a key role in the development of diabetes-induced cognitive impairment. However, strategies to inhibit NLRP3 inflammasome activation remain elusive. Herein, we evaluated the impact of a walnut-derived peptide, TWLPLPR (TW-7), on cognitive impairment in high-fat diet/streptozotocin-induced type 2 diabetes mellitus (T2DM) mice and explored its underlying mechanisms in high glucose-induced HT-22 cells. In the Morris water maze test, TW-7 alleviated cognitive deficits in mice; this was confirmed at the level of synaptic structure and dendritic spine density in the mouse hippocampus using transmission electron microscopy and Golgi staining. TW-7 increased the expression of synaptic plasticity-related proteins and suppressed the NEK7/NLRP3 inflammatory pathway, as determined by western blotting and immunofluorescence analysis. The mechanism of action of TW-7 was verified in an HT-22 cell model of high glucose-induced insulin resistance. Collectively, TW-7 could regulate T2DM neuroinflammation and synaptic function-induced cognitive impairment by inhibiting NLRP3 inflammasome activation and improving synaptic plasticity.

Asunto(s)

Disfunción Cognitiva , Diabetes Mellitus Tipo 2 , Juglans , Ratones , Animales , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Inflamasomas/metabolismo , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Juglans/metabolismo , Disfunción Cognitiva/tratamiento farmacológico , Disfunción Cognitiva/metabolismo , Glucosa

RESUMEN

This study aimed to utilize zinc coordination to promote the hypoglycemic and antioxidant properties of walnut-derived peptides, such as walnut protein hydrolysate (WPH) and Leu-Pro-Leu-Leu-Arg (LPLLR, LP5), of which LP5 was previously identified from WPH. The optimal conditions for the chelation were a peptide-to-zinc ratio of 6:1, pH of 9, duration of 50 min, and temperature of 50 °C. The WPH-Zn and LP5-Zn complexes increased the α-glucosidase inhibition, α-amylase inhibition, and antioxidant activity more than WPH and LP5 (p < 0.05). In particular, the antioxidant activity of WPH-Zn was superior to LP5-Zn. This is attributable to the WPH containing more aromatic amino acids, carboxylate groups and the imidazole groups, which implies its capacity to potentially coordinate with Zn2+ to form the WPH-Zn complex. Moreover, particle size, zeta potential, and scanning electron microscope indicated that the chelation of Zn2+ by peptides led to intramolecular and intermolecular folding and aggregation.

Asunto(s)

Juglans , Juglans/química , Antioxidantes/farmacología , Zinc/química , Control Glucémico , Péptidos/farmacología , Quelantes , Hidrolisados de Proteína/química

RESUMEN

We investigated the absorption mechanism of the shrimp peptide QMDDQ in small intestines, explored its physiological function in inhibiting neuronal hyperactivity, and verified its entry into the brain in vivo to display functional activity. The everted rat sac model and a Caco-2 paracellular absorption monolayer model were used, indicating that QMDDQ has a good absorption capacity with an apparent permeability coefficient (Papp) > 1 × 10-6 cm/s and the absorption of QMDDQ was concentration-dependent. When the concentration of QMDDQ was 1 mM and the transport time was 180 min, the highest absorption concentration of QMDDQ was 41.17 ± 3.48 µM (P < 0.05). The myosin light-chain kinase (MLCK)-specific inhibitor ML-7 and activator MPA, Western blotting, and immunofluorescence results showed that QMDDQ absorption takes place by mediating the MLCK-p-MLCK-MLC signaling pathway, reversibly opening the zonula occludens-1 (ZO-1), occludin in tight junctions (TJs), upregulating claudin-2 expression, and reaching targets through blood to inhibit neuronal overactivity. Results of fluorescence imaging in vivo verified that QMDDQ could enter the brain 4 h after oral administration. The results provide a theoretical foundation for the mechanism of paracellular absorption of active peptides and a starting point for the development of functional foods for Alzheimer's disease intervention.

Asunto(s)

Mucosa Intestinal , Cadenas Ligeras de Miosina , Humanos , Ratas , Animales , Células CACO-2 , Mucosa Intestinal/metabolismo , Ocludina/metabolismo , Péptidos/metabolismo , Uniones Estrechas/metabolismo

RESUMEN

Food-derived peptides, as dietary supplements, have significant effects on promoting brain health and relieving central nervous system (CNS) diseases. However, the blood-brain barrier (BBB) greatly limits their in-brain bioavailability. Thus, overcoming the BBB to target the CNS is a major challenge for bioactive peptides in the prevention and treatment of CNS diseases. This review discusses improvement in the neuroprotective function of food-derived active peptides in CNS diseases, as well as the source of BBB penetrating peptides (BBB-shuttles) and the mechanism of transmembrane transport. Notably, this review also discusses various peptide modification methods to overcome the low permeability and stability of the BBB. Lipification, glycosylation, introduction of disulfide bonds, and cyclization are effective strategies for improving the penetration efficiency of peptides through the BBB. This review provides a new prospective for improving their neuroprotective function and developing treatments to delay or even prevent CNS diseases.

Asunto(s)

Barrera Hematoencefálica , Enfermedades del Sistema Nervioso Central , Humanos , Barrera Hematoencefálica/metabolismo , Estudios Prospectivos , Encéfalo/metabolismo , Péptidos/metabolismo , Enfermedades del Sistema Nervioso Central/tratamiento farmacológico , Enfermedades del Sistema Nervioso Central/prevención & control , Transporte Biológico

RESUMEN

In this study, we investigated the protective mechanism of walnut-derived peptide LPLLR (LP-5) against cognitive impairment induced in a dextran sodium sulfate (DSS)-induced colitis mouse model, with emphasis on the microbiota-gut-brain axis (MGBA). The results revealed that LP-5 could improve the learning ability and memory of mice with cognitive impairment and mitigate colitis symptoms, including weight loss, bloody stools, colon shortening, and histopathological changes. Additionally, LP-5 protected the integrity of the intestinal barrier by promoting the expression of tight junction proteins (TJs) while attenuating colonic inflammation by suppressing proinflammatory cytokine and epithelial cell apoptosis. Western blotting indicated that LP-5 treatment suppressed the inflammatory NF-κB/MLCK/MLC signaling pathway activity. Furthermore, LP-5 ameliorated hippocampal neuron damage and protected blood-brain barrier (BBB) integrity by downregulating microglia marker protein Iba-1, increasing TJ protein expression, and restoring the deterioration of synaptic proteins. Importantly, 16S rRNA sequencing results indicated that LP-5 reshaped the abundance of a wide range of gut microbiota at the phylum and genus levels, with increased Prevotella and Akkermansia associated with tryptophan (TRP), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA). These findings suggest that LP-5 could maintain intestinal barrier and BBB integrity, reverse gut dysbiosis, and improve learning and memory ability in colitis mice, providing novel insights into alterations of gut microbes in colitis and a potential new mechanism by which it causes cognitive impairment.

Asunto(s)

Disfunción Cognitiva , Colitis , Juglans , Animales , Ratones , Dextranos/metabolismo , Eje Cerebro-Intestino , ARN Ribosómico 16S , Colitis/inducido químicamente , Colitis/tratamiento farmacológico , Colitis/genética , Colon/metabolismo , Citocinas/metabolismo , Serotonina/metabolismo , Disfunción Cognitiva/tratamiento farmacológico , Disfunción Cognitiva/genética , Disfunción Cognitiva/metabolismo , Sulfato de Dextran/efectos adversos , Sulfato de Dextran/metabolismo , Ratones Endogámicos C57BL , Modelos Animales de Enfermedad

RESUMEN

The complement pathway is a major component of the innate immune system, which is critical for recognizing and clearing pathogens that rapidly react to defend the body against external pathogens. Many components of this pathway are expressed throughout the brain and play a beneficial role in synaptic pruning in the developing central nervous system (CNS). However, excessive complement-mediated synaptic pruning in the aging or injured brain may play a contributing role in a wide range of neurodegenerative diseases. Complement Component 1q (C1q), an initiating recognition molecule of the classical complement pathway, can interact with a variety of ligands and perform a range of functions in physiological and pathophysiological conditions of the CNS. This review considers the function and immunomodulatory mechanisms of C1q; the emerging role of C1q on synaptic pruning in developing, aging, or pathological CNS; the relevance of C1q; the complement pathway to neurodegenerative diseases; and, finally, it summarizes the foods with beneficial effects in neurodegenerative diseases via C1q and complement pathway and highlights the need for further research to clarify these roles. This paper aims to provide references for the subsequent study of food functions related to C1q, complement, neurodegenerative diseases, and human health.

RESUMEN

L-aspartic acid, L-threonine, L-isoleucine, l-lysine, and L-methionine constitute the l-aspartate amino acids (AFAAs). Except for L-aspartic acid, these are essential amino acids that cannot be synthesized by humans or animals themselves. E. coli and C. glutamicum are the main model organisms for AFAA production. It is necessary to reconstitute microbial cell factories and the physiological state of industrial fermentation cells for in-depth research into strains with higher AFAA production levels and optimal growth states. Considering that the anabolic pathways of the AFAAs and engineering modifications have rarely been reviewed in the latest progress, this work reviews the central metabolic pathways of two strains and strategies for the metabolic engineering of AFAA synthetic pathways. The challenges posed by microbial physiology in AFAA production and possible strategies to address them, as well as future research directions for constructing strains with high AFAA production levels, are discussed in this review article.

Asunto(s)

Aminoácidos , Corynebacterium glutamicum , Humanos , Aminoácidos/metabolismo , Ácido Aspártico/metabolismo , Ingeniería Metabólica , Escherichia coli/genética , Escherichia coli/metabolismo , Corynebacterium glutamicum/metabolismo , Fermentación

RESUMEN

A novel calcium-binding peptide was purified from peanut protein hydrolysate using gel filtration chromatography and identified using HPLC-MS/MS. Its amino acid sequence was determined as Phe-Pro-Pro-Asp-Val-Ala (FPPDVA, named as FA6) with the calcium-binding capacity of 15.67 ± 0.39 mg/g. Then, the calcium chelating characteristics of FPPDVA were investigated using ultraviolet-visible absorption spectroscopy, fluorescence spectroscopy, Fourier transform infrared spectroscopy, particle size, and zeta potential. The results showed that FPPDVA interacted with calcium ions, the chelation of calcium ions induced FPPDVA to fold and form a denser structure, the calcium-binding sites may mainly involve oxygen atoms from the carboxyl residues of Asp and Ala, and Phe possessed contact energy and carbonyl residues of Val. Microstructure analysis showed that FPPDVA-calcium chelate exhibited a regularly ordered and tightly aggregated sheets or block structures. Additionally, FPPDVA-calcium chelate had good gastrointestinal digestive stability and thermal stability. The results of everted rat intestinal sac and Caco-2 cell monolayer experiments showed that FPPDVA-calcium chelate could promote calcium absorption and transport through the Cav1.3 and TRPV6 calcium channels. These data suggest that FPPDVA-calcium chelate possesses the potential to be developed and applied as calcium supplement.

Asunto(s)

Arachis , Calcio , Humanos , Animales , Ratas , Calcio/metabolismo , Arachis/metabolismo , Hidrolisados de Proteína/química , Células CACO-2 , Espectrometría de Masas en Tándem , Péptidos/química , Calcio de la Dieta/metabolismo , Quelantes/química , Iones

RESUMEN

This work aimed to investigate whether there are synergistic effects between walnut peptide (WNP) and ginseng extracts (GSE) treatments to ameliorate the memory impairment caused by scopolamine (SCOP). The Morris water maze trial, hippocampal neuron morphology, neurotransmitters, and synaptic ultrastructure were examined, along with brain-derived neurotrophic factor (BDNF)-related signaling pathway proteins. The results of the Morris water maze trial demonstrated that the combined administration of WNP and GSE effectively alleviated memory impairment in C57BL/6 rats caused by SCOP. Improvement in the morphology of hippocampal neurons, dendritic spines, and synaptic plasticity and upregulation of neurotransmitters AChE, ACh, ChAT, Glu, DA, and 5-HT supported the memory improvement effects of WNP + GSE. In addition, compared with the model group, WNP + GSE significantly enhanced the protein levels of VAChT, Trx-1, and the CREB/BDNF/TrkB pathway in hippocampal and PC12 cells induced by SCOP (p < 0.05). Notably, WNP + GSE boosted memory via multiple pathways, not only the BDNF/TrkB/CREB target.