Novel Peptides from Sturgeon Ovarian Protein Hydrolysates Prevent Oxidative Stress-Induced Dysfunction in Osteoblast Cells: Purification, Identification, and Characterization.

This study aimed to explore antioxidant peptides derived from sturgeon (Acipenser schrenckii) ovaries that exhibit antiosteoporotic effects in oxidative-induced MC3T3-E1 cells. The F3-15 component obtained from sturgeon ovarian protein hydrolysates (SOPHs) via gel filtration and RP-HPLC significantly increased the cell survival rate (from 49.38 ± 2.88 to 76.26 ± 2.09%). Two putative antioxidant-acting peptides, FDWDRL (FL6) and FEGPPFKF (FF8), were screened from the F3-15 faction via liquid chromatography-tandem mass spectrometry (LC-MS/MS) and through prediction by computer simulations. Molecular docking results indicated that the possible antioxidant mechanisms of FL6 and FF8 involved blocking the active site of human myeloperoxidase (hMPO). The in vitro tests showed that FL6 and FF8 were equally adept at reducing intracellular ROS levels, increasing the activity of antioxidant enzymes, and protecting cells from oxidative injuries by inhibiting the mitogen-activated protein kinase (MAPK) pathway and activating the phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase-3ß (GSK-3ß) signaling pathway. Moreover, both peptides could increase differentiation and mineralization abilities in oxidatively damaged MC3T3-E1 cells. Furthermore, FF8 exhibited high resistance to pepsin and trypsin, showcasing potential for practical applications.

Unlocking the health potential of anthocyanins: a structural insight into their varied biological effects.

Anthocyanins have become increasingly important to the food industry due to their colorant features and many health-promoting activities. Numerous studies have linked anthocyanins to antioxidant, anti-inflammatory, anticarcinogenic properties, as well as protection against heart disease, certain types of cancer, and a reduced risk of diabetes and cognitive disorders. Anthocyanins from various foods may exhibit distinct biological and health-promoting activities owing to their structural diversity. In this review, we have collected and tabulated the key information from various recent published studies focusing on investigating the chemical structure effect of anthocyanins on their stability, antioxidant activities, in vivo fate, and changes in the gut microbiome. This information should be valuable in comprehending the connection between the molecular structure and biological function of anthocyanins, with the potential to enhance their application as both colorants and functional compounds in the food industry.

Chicoric Acid Effectively Mitigated Dextran Sulfate Sodium (DSS)-Induced Colitis in BALB/c Mice by Modulating the Gut Microbiota and Fecal Metabolites.

Chicoric acid (CA) has been reported to exhibit biological activities; it remains unclear, however, whether CA could regulate colitis via modulation of the gut microbiota and metabolites. This study aimed to assess CA's impact on dextran sulfate sodium (DSS)-induced colitis, the gut microbiota, and metabolites. Mice were induced with 2.5% DSS to develop colitis over a 7-day period. CA was administered intragastrically one week prior to DSS treatment and continued for 14 days. The microbial composition in the stool was determined using 16S rRNA sequencing, while non-targeted metabolomics was employed to analyze the metabolic profiles of each mouse group. The results show that CA effectively alleviated colitis, as evidenced by an increased colon length, lowered disease activity index (DAI) and histological scores, and decreased tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) expression levels. CA intervention restored the structure of gut microbiota. Specifically, it decreased the abundance of Bacteroidetes and Cyanobacteria at the phylum level and Bacteroides, Rosiarcus, and unclassified Xanthobacteraceae at the genus level, and increased the abundance of unclassified Lachnospiraceae at the genus level. Metabolomic analysis revealed that CA supplementation reversed the up-regulation of asymmetric dimethylarginine, N-glycolylneuraminic acid, and N-acetylneuraminic acid, as well as the down-regulation of phloroglucinol, thiamine, 4-methyl-5-thiazoleethanol, lithocholic acid, and oxymatrine induced by DSS. Our current research provides scientific evidence for developing CA into an anti-colitis functional food ingredient. Further clinical trials are warranted to elucidate the efficacy and mechanism of CA in treating human inflammatory bowel disease (IBD).

Recent advances in pulse protein conjugation and complexation with polyphenols: an emerging approach to improve protein functionality and health benefits.

Pulses have attracted much attention in the food industry due to their low cost, high yield, and high protein content, which promises to be excellent alternative protein sources. Recently, techniques for covalent and noncovalent binding of pulse proteins to polyphenols are expected to solve the problem of their poor protein functional properties. Additionally, these conjugates and complexes also show several health benefits. This review summarizes the formation of conjugates and complexes between pulse proteins and polyphenols through covalent and noncovalent binding and the impact of this structural change on protein functionalities and potential health benefits. Recent studies show that pulse protein functionalities can be influenced by polyphenol dose. This is mainly the case for adverse effects on solubility and enhancement in emulsifying capacity. Also, the conjugates/complexes exhibit antioxidant activity and can alter protein digestibility. The antioxidant activity of polyphenols could be retained after binding to proteins, while the effect on digestibility depends on the type or dosage of polyphenols. Considering the link between polyphenols and their potential health benefits, pulse polyphenols would be a good choice for producing the conjugates/complexes due to their low cost and proven potential benefits. Further studies on the structure-function-health benefits relationship of pulse protein-polyphenol conjugates and complexes are still required, as well as the validation of their application as functional foods in the food industry.

CYP eicosanoid pathway mediates colon cancer-promoting effects of dietary linoleic acid.

Human and animal studies support that consuming a high level of linoleic acid (LA, 18:2ω-6), an essential fatty acid and key component of the human diet, increases the risk of colon cancer. However, results from human studies have been inconsistent, making it challenging to establish dietary recommendations for optimal LA intake. Given the importance of LA in the human diet, it is crucial to better understand the molecular mechanisms underlying its potential colon cancer-promoting effects. Using LC-MS/MS-based targeted lipidomics, we find that the cytochrome P450 (CYP) monooxygenase pathway is a major pathway for LA metabolism in vivo. Furthermore, CYP monooxygenase is required for the colon cancer-promoting effects of LA, since the LA-rich diet fails to exacerbate colon cancer in CYP monooxygenase-deficient mice. Finally, CYP monooxygenase mediates the pro-cancer effects of LA by converting LA to epoxy octadecenoic acids (EpOMEs), which have potent effects on promoting colon tumorigenesis via gut microbiota-dependent mechanisms. Overall, these results support that CYP monooxygenase-mediated conversion of LA to EpOMEs plays a crucial role in the health effects of LA, establishing a unique mechanistic link between dietary fatty acid intake and cancer risk. These results could help in developing more effective dietary guidelines for optimal LA intake and identifying subpopulations that may be especially vulnerable to LA's negative effects.

Production, purification, and functional properties of microbial fibrinolytic enzymes produced by microorganism obtained from soy-based fermented foods: developments and challenges.

According to the World Health Organization, cardiovascular disease (CVD) has become a major cause of chronic illness around the globe. It has been reported that soy-based fermented food (SFF) is very effective in preventing thrombus (one of the most important contributing factors to CVD), which are mainly attributed to the bioactive substances, especially the fibrinolytic enzymes (FE) generated by microorganisms during the fermentation process of soybean food. This paper therefore mainly reviewed the microbial fibrinolytic enzymes (MFE) from SFF. We first discuss the use of microbial fermentation to produce FE, with an emphasis on the strains involved. The production, purification, physicochemical properties, structure-functional attributes, functional properties and possible application of MFE from SFF are then discussed. Finally, current limitations and future perspectives for the production, purification, and the practical application of MFE are discussed. MFE from SFF pose multiple health benefits, including thrombolysis, antihypertension, anti-inflammatory, anti-hyperlipidemia, anticancer, neuroprotective, antiviral and other activities. Therefore, they exhibit great potential for functional foods and nutraceutical applications, especially foods with CVDs prevention potential.

Comparative Effects of Traditional Versus Genetically Modified Soybean Oils on Colon Tumorigenesis in Mice.

Soybean oil, which has high abundance of linoleic acid (LA, 18:2ω-6), is the most commonly consumed edible oil. Recent studies support that a high dietary intake of LA is linked with increased risks of developing colonic inflammation and colon cancer. Here we studied the effects of the genetically modified Plenish® soybean oil, which has low abundance of LA as well as α-linolenic acid (ALA, 18:3ω-3), on development of azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colon tumorigenesis in mice. Compared with a diet rich in traditional soybean oil, administration of a diet enriched with the Plenish oil has little impact on AOM/DSS-induced colon tumorigenesis, colonic infiltration of immune cells, expressions of inflammatory genes, and tumor markers. These results suggest that the traditional and the Plenish soybean oils have similar effects on development of AOM/DSS-induced colon cancer in mice.

Bisphenol-A exposure leads to neurotoxicity through upregulating the expression of histone deacetylase 2 in vivo and in vitro.

Bisphenol-A (BPA), an environmental endocrine disruptor, is toxic to the central nervous system. Although recent studies have shown BPA-induced neurotoxicity, it is far from clear what precisely epigenetic mechanisms are involved in BPA-induced cognitive deficits. In this study, pheochromocytoma (PC12) cells were treated with BPA at 1 µM for 36 h in vitro. In vivo, C57BL/6 mice were administered to BPA at a dose of 1 mg/kg/day for 10 weeks. The results showed that 1 µM BPA exposure for 36 h impaired neurite outgrowth of PC12 cells through decreasing the primary and secondary branches. Besides, BPA exposure decreased the level of Ac-H3K9 (histone H3 Lys9 acetylation) by upregulating the expression of HDAC2 (histone deacetylases 2) in PC12 cells. Furthermore, treatment of both TSA (Trichostatin A, inhibitor of the histone deacetylase) and shHDAC2 plasmid (HDAC2 knockdown construct) resulted in amelioration neurite outgrowth deficits induced by BPA. In addition, it was shown that repression of HDAC2 could markedly rescue the spine density impairment in the hippocampus and prevent the cognitive impairment caused by BPA exposure in mice. Collectively, HDAC2 plays an essential role in BPA-induced neurotoxicity, which provides a potential molecular target for medical intervention.

Sweet tea (Lithocarpus polystachyus rehd.) as a new natural source of bioactive dihydrochalcones with multiple health benefits.

Sweet tea (Lithocarpus polystachyus Rehd.) has been consumed as herbal tea to prevent and manage diabetes for a long time. Recent studies indicate that sweet tea is rich in a variety of bioactive compounds, especially a class of nonclassical flavonoids, dihydrochalcones. In order to provide a better understanding of sweet tea and its main dihydrochalcones on human health, this review mainly summarizes related literature in the recent ten years, with the potential molecular mechanisms emphatically discussed. Phlorizin, phloretin, and trilobatin, three natural sweeteners, are the main dihydrochalcones in sweet tea. In addition, sweet tea and its dihydrochalcones exhibit plenty of health benefits, such as antioxidant, anti-inflammatory, antimicrobial, cardioprotective, hepatoprotective, antidiabetic, and anticancer effects, which are associated with the regulation of different molecular targets and signaling pathways. Therefore, sweet tea, as a rare natural source of dihydrochalcones, can be processed and developed into nutraceuticals or functional foods, with the potential application in the prevention and management of certain chronic diseases.

Plant-Based Foods and Their Bioactive Compounds on Fatty Liver Disease: Effects, Mechanisms, and Clinical Application.

Fatty liver disease (FLD), including nonalcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (AFLD), is a serious chronic metabolic disease that affects a wide range of people. Lipid accumulation accompanied by oxidative stress and inflammation in the liver is the most important pathogenesis of FLD. The plant-based, high-fiber, and low-fat diet has been recommended to manage FLD for a long time. This review discusses the current state of the art into the effects, mechanisms, and clinical application of plant-based foods in NAFLD and AFLD, with highlighting related molecular mechanisms. Epidemiological evidence revealed that the consumption of several plant-based foods was beneficial to alleviating FLD. Further experimental studies found out that fruits, spices, teas, coffee, and other plants, as well as their bioactive compounds, such as resveratrol, anthocyanin, curcumin, and tea polyphenols, could alleviate FLD by ameliorating hepatic steatosis, oxidative stress, inflammation, gut dysbiosis, and apoptosis, as well as regulating autophagy and ethanol metabolism. More importantly, clinical trials confirmed the beneficial effects of plant-based foods on patients with fatty liver. However, several issues need to be further studied especially the safety and effective doses of plant-based foods and their bioactive compounds. Overall, certain plant-based foods are promising natural sources of bioactive compounds to prevent and alleviate fatty liver disease.

Ameliorative effects of L-arginine? On heat-induced phase separation of Aristichthys nobilis myosin are associated with the absence of ordered secondary structures of myosin.

This investigation aimed to study the potential mechanism of L-arginine (L-Arg) on the heat-induced phase separation phenomenon of myosin from the perspective of conformational changes of myosin. L-Arg ameliorated the phase separation of myosin after a two-step heating procedure via suppression of heat-induced aggregation of myosin. The effect of L-Arg on the heating of myosin at high temperatures (75-85 °C) was more pronounced than that in the setting stage (35-45 °C), suggesting that the ameliorative effects of L-Arg on the heat-induced phase separation of myosin are mainly attributed to the inhibition of rod-rod cross-linking between denatured myosin molecules. Additionally, L-Arg without pH modification exhibited an increased ability to suppress the gelation of myosin compared with pH modification, indicating that both pH effects and the particular structure of L-Arg play noticeable roles in the suppression of myosin gelation. Far-UV circular dichroism, intrinsic fluorescence spectroscopy and differential scanning calorimetry demonstrated that L-Arg induced the absence of ordered secondary structures of myosin molecules, especially ß-sheets, and thus generated a looser protein structure, which may represent the dominant suppression mechanisms of L-Arg on the heat-induced aggregation of myosin. This work provided support for the use of L-Arg as a food additive, and the results of this study will be attractive to the meat and beverage products.

Absorption, metabolism, and bioactivity of vitexin: recent advances in understanding the efficacy of an important nutraceutical.

vitexin, an apigenin-8-C-glucoside, is widely present in numerous edible and medicinal plants. vitexin possesses a variety of bioactive properties, including antioxidation, anti-inflammation, anti-cancer, neuron-protection, and cardio-protection. Other beneficial health effects, such as fat reduction, glucose metabolism, and hepatoprotection, have also been reported in recent studies. This review briefly discusses the absorption and metabolism of vitexin, as well as its influence on gut microbiota. Recent advances in understanding the pharmacological and biological effects of vitexin are then reviewed. Improved knowledge of the absorption, metabolism, bioactivity, and molecular targets of vitexin is crucial for the better utilization of this emerging nutraceutical as a chemopreventive and chemotherapeutic agent.

Use of l-arginine-assisted ultrasonic treatment to change the molecular and interfacial characteristics of fish myosin and enhance the physical stability of the emulsion.

The effects of l-arginine (Arg)-assisted ultrasonic treatment on the molecular and interfacial characteristics of myosin and emulsifying properties of the emulsion were evaluated to ascertain the underlying mechanism in improving the emulsion stability. Ultrasonication induced the exposure of residues of native myosin, which was increased by the addition of Arg (40 mM). Furthermore, in terms of emulsions containing Arg, the higher the ultrasonication intensity was, the greater the increase in adsorbed protein (from 15.43 ± 0.28% to 50.49 ± 1.65%) and π value, and the decrease in droplet sizes (from 4098 nm to 2324 nm) (P < 0.05). Moreover, the increase in the ordered structures of interfacial myosin induced by Arg and ultrasonication favoured the formation of a protein gelation network. In summary, Arg-assisted ultrasonic treatment improved the stability of the emulsion by inducing the exposure of native myosin and facilitating the formation of ordered structures of interfacial myosin.

Effects of l-arginine and l-histidine on heat-induced aggregation of fish myosin: Bighead carp (Aristichthys nobilis).

This research focused on the effects of l-arginine (l-Arg) and l-histidine (l-His) on the heat-induced aggregation of fish myosin. l-Arg/l-His increased the pH of the myosin solution from 6.82 to 8.74 and 7.24, respectively, and decreased the turbidity, aggregate size, shear modulus, and breaking force. The incorporation of l-Arg/l-His decreased the surface hydrophobicity during setting, but increased it during the two-step heating. The heat-induced aggregation of myosin was suppressed by both amino acids, with the inhibitory effect being greater for l-Arg than l-His. On one hand, the change in the pH played a critical role in suppressing the heat-induced aggregation of myosin. On the other hand, the characteristics of l-Arg/l-His themselves, such as net charges and particular R-groups, were another main contributor to aggregation suppression. Particularly, l-Arg/l-His could interact with exposed aromatic residues of myosin, and the interactions may dominate and overwhelm the burial of aromatic residues during two-step heating.

Vitexin ameliorates high fat diet-induced obesity in male C57BL/6J mice via the AMPKα-mediated pathway.

Vitexin, a bioactive compound isolated from hawthorn leaf extracts, has been reported to exhibit many biological activities, such as anticancer, antioxidation, and adipogenesis inhibition activities. The current study explored the effects of vitexin on high fat diet (HFD)-induced obesity/adipogenesis in male C57BL/6J mice and 3T3-L1 adipocytes, as well as the underlying mechanisms thereof. Vitexin significantly mitigated HFD-induced body weight gain and adiposity. Vitexin also partially normalized serum, hepatic lipid contents, and decreased adipocyte size induced by the HFD. Consistently, there were significant effects of vitexin on important regulators of lipid metabolism, including AMP-activated protein kinase-α (AMPKα), CAATT element binding protein-α (C/EBPα), and fatty acid synthase (FAS) in white adipose tissue. Moreover, vitexin significantly inhibited fat accumulation in 3T3-L1 adipocytes, and this was totally abolished by compound C (an AMPKα inhibitor). These results suggest that vitexin may prevent HFD-induced obesity/adipogenesis via the AMPKα mediated pathway.

AAK-2 and SKN-1 Are Involved in Chicoric-Acid-Induced Lifespan Extension in Caenorhabditis elegans.

Chicoric acid is a dicaffeoyl ester with many bioactivities, including antioxidation, antidiabetes, and anti-inflammation. A previous study reported that chicoric acid extended the lifespan in Caenorhabditis elegans; however, the mechanism behind the effect of chicoric acid on the extended lifespan remains unknown. Consistent with the previous report, chicoric acid (25 and 50 µM) extended the maximum lifespan compared to the control (17.5 ± 3.3 and 15.6 ± 5%, respectively; p < 0.001 for both). The declines of the pumping rate and locomotive activity, two indicators of aging, were delayed by chicoric acid. Moreover, chicoric acid enhanced resistance to oxidative stress in C. elegans. It was further determined that the extended lifespan by chicoric acid was in part via aak-2 [a homologue of adenosine monophosphate (AMP)-activated protein kinase] and skn-1 (a homologue of nuclear factor erythroid 2-related factor 2). The current findings suggest that chicoric acid has the potential to be used as an anti-aging bioactive compound.

Flubendiamide Enhances Adipogenesis and Inhibits AMPKα in 3T3-L1 Adipocytes.

Flubendiamide, a ryanoid class insecticide, is widely used in agriculture. Several insecticides have been reported to promote adipogenesis. However, the potential influence of flubendiamide on adipogenesis is largely unknown. The current study was therefore to determine the effects of flubendiamide on adipogenesis utilizing the 3T3-L1 adipocytes model. Flubendiamide treatment not only enhanced triglyceride content in 3T3-L1 adipocytes, but also increased the expression of cytosine-cytosine-adenosine-adenosine-thymidine (CCAAT)/enhancer-binding protein α and peroxisome proliferator-activated receptor gamma-γ, two important regulators of adipocyte differentiation. Moreover, the expression of the most important regulator of lipogenesis, acetyl coenzyme A carboxylase, was also increased after flubendiamide treatment. Further study revealed that 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or A769662, two Adenosine 5'-monophosphate (AMP)-activated protein kinase α activators, subverted effects of flubendiamide on enhanced adipogenesis. Together, these results suggest that flubendiamide promotes adipogenesis via an AMPKα-mediated pathway.

Permethrin decreased insulin-stimulated AKT phosphorylation dependent on extracellular signal-regulated kinase-1 (ERK), but not AMP-activated protein kinase α (AMPKα), in C2C12 myotubes.

Previously 10 µM permethrin (38.7% cis and 59.4% trans isomers), a pyrethroid insecticide widely used in agriculture and household products for pest control, was reported to reduce insulin-stimulated glucose uptake and phosphorylation of protein kinase B (p-AKT) in C2C12 mouse myotubes. The underlying mechanisms on how permethrin decreases insulin-stimulated AKT phosphorylation, however, are unknown. Thus, the goal of this study was to determine the possible mechanism(s) through which permethrin reduced insulin-stimulated AKT phosphorylation in C2C12 myotubes. Permethrin treatment, at 10 µM, decreased insulin-stimulated membrane glucose transporter type 4 (GLUT4) and AKT phosphorylation, and increased insulin receptor substrate 1 (IRS1) Ser307 phosphorylation in the presence of insulin. The inactivation of AKT by permethrin was independent of AMPKα. ERK inactivation by U0126, however, restored insulin-stimulated AKT phosphorylation, which was decreased by permethrin treatment. These results suggest that permethrin decreased insulin-stimulated AKT phosphorylation via ERK activation, but not by AMPKα inactivation.

Imidacloprid Promotes High Fat Diet-Induced Adiposity in Female C57BL/6J Mice and Enhances Adipogenesis in 3T3-L1 Adipocytes via the AMPKα-Mediated Pathway.

Imidacloprid, a neonicotinoid insecticide, was previously reported to enhance adipogenesis and resulted in insulin resistance in cell culture models. It was also reported to promote high fat diet-induced obesity and insulin resistance in male C57BL/6J mice. Thus, the goal of the present study was to determine the effects of imidacloprid and dietary fat interaction on the development of adiposity and insulin resistance in female C57BL/6J mice. Mice were fed with a low (4% w/w) or high fat (20% w/w) diet containing imidacloprid (0.06, 0.6, or 6 mg/kg bw/day) for 12 weeks. Mice fed with imidacloprid (0.6 mg/kg bw/day) significantly enhanced high fat diet-induced weight gain and adiposity. Treatment with imidacloprid significantly increased serum insulin levels with high fat diet without effects on other markers of glucose homeostasis. AMPKα activation was significantly inhibited by 0.6 and 6 mg imidacloprid/kg bw/day in white adipose tissue. Moreover, AMPKα activation with 5-aminoimidazole-4-carboxamide ribonucleotide abolished the effects of imidacloprid (10 µM) on enhanced adipogenesis in 3T3-L1 adipocytes. N-Acetyl cysteine also partially reversed the effects of imidacloprid on reduced phosphorylation of protein kinase B (AKT) in C2C12 myotubes. These results indicate that imidacloprid may potentiate high fat diet-induced adiposity in female C57BL/6J mice and enhance adipogenesis in 3T3-L1 adipocytes via the AMPKα-mediated pathway. Imidacloprid might also influence glucose homeostasis partially by inducing cellular oxidative stress in C2C12 myotubes.

Preventive effects of cranberry products on experimental colitis induced by dextran sulphate sodium in mice.

With the prevalence of inflammatory bowel disease (IBD) and its associated risk for development of colorectal cancer, it is of great importance to prevent and treat IBD. However, due to the complexity of etiology and potentially serious adverse effects, treatment options for IBD are relatively limited. Thus, the purpose of this study was to identify a safe food-based approach for the prevention and treatment of IBD. In this study, we tested the effects of cranberry products on preventing dextran sulphate sodium-induced murine colitis. Our results suggest that both cranberry extract and dried cranberries-fed groups had a significantly reduced disease activity index, where dried cranberries were more effective in preventing colitis than cranberry extract. Shortening of colon length, colonic myeloperoxidase activity and production of pro-inflammatory cytokines were attenuated in animals fed dried cranberries compared to the controls. The current report suggests that cranberries can be applied to prevent and reduce the symptoms of IBD.