Exposure to alcohol caused toxicity in Caenorhabditis elegans (C. elegans). However, the underlying mechanisms for this induced toxicity by alcohol remain largely unclear. We examined possible association of ferroptosis activation with toxicity of alcohol. This study revealed that alcohol (400 mM-700 mM)-related iron toxicity suppressed head thrash, pharyngeal pumping of C. elegans, generated reproductive toxicity and oxidative stress, while rescued by ferroptosis inhibitor Fer-1(100 μmol/L) and iron chelating agent DFO (50 μmol/L). Meanwhile, alcohol resulted in increased Fe²⁺ levels due to iron metabolism dysfunction, promoting iron uptake by increasing gene level of Smf-3, suppressing iron storage and efflux by decreasing gene level of Ftn-1 and Fpn-1.1. Besides, alcohol caused increased MDA content, decreased GSH content, as well as alterations in the expression Gpx-1, Ftn-1, and Acs-17, facilitating ferroptosis. Moreover, alcohol-caused shorten lifespan, abnormal physiological state, reproductive toxicity as well as disturbed iron homeostasis and ferroptosis were all exacerbated in hsf-1 and skn-1 mutation C. elegans. The study offers novel insights into the mechanisms of alcohol-induced iron metabolism dysfunction and ferroptosis in C. elegans.

Food-grade methyl cinnamate as an acyl donor was used to enzymatically acylate cyanidin-3-O-glucoside (C3G) under reduced pressure, which has the advantages of safety, high efficiency and single acylation product. After being purified by semi-preparative high-performance liquid chromatography (SP-HPLC), the acylation product was evaluated for its thermal stability and antioxidant activity. The results showed that the acylation rate was 80%, and the purity of the purified acylated C3G was as high as 98.3%. Mass spectral analysis showed that the acylated product was cyanidin-3-(6-cinnamoyl)-glucoside (C3(6C)G). Acylation modification significantly improved the lipid solubility and thermal stability of C3G. C3G and C3(6C)G had weaker scavenging capacity against 2,2-amino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical cation but similar 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging capacity, ferric reducing and antioxidant power (FRAP) and hydroxyl radical scavenging capacity compared with vitamin C (VC) at the same concentration. At 200 μmol/L, the hydroxyl and DPPH radical scavenging capacity of C3(6C)G was significantly enhanced compared with C3G (P < 0.05), while there was no significant difference in ABTS radical cation scavenging or FRAP between C3G and C3(6C)G (P > 0.05), which showed that cinnamyl modification did not impair the antioxidant capacity of anthocyanins, but instead improved the scavenging capacity against hydroxyl radicals.

This study aimed to use the Gene Expression Omnibus (GEO) database combined with network pharmacology technology to investigate the positive effect of galangin on alcoholic fatty liver disease (AFLD) and explore its potential mechanism. The study first screened the differential genes in ALFD mice through the GEO database, obtained the possible targets of galangin through the SwissTargetPrediction and PharmMapper databases, and then obtained the intersection of drug and disease targets through a Venn diagram to build a “drug-target-pathway-disease” network relationship diagram, and its possible molecular mechanisms were analyzed through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. The network pharmacology analysis identified 22 potential targets for galangin in the treatment of AFLD, and protein-protein interaction network analysis revealed that the top 5 targets were protein kinase B (AKT) 1, epidermal growth factor receptor, mitogen-activated protein kinase (MAPK) 3, myeloid cell leukemia 1, and KIT proto-oncogene receptor tyrosine kinase. The KEGG results showed that the treatment of AFLD by galangin may be related to the MAPK signaling pathway, cyclic adenosine monophosphate signaling pathway, Ras-related protein 1 signaling pathway and phosphoinositide 3 kinase/AKT signaling pathway. Therefore, the combination of GEO database and network pharmacology prediction results showed that galangin could alleviate alcoholic fatty liver and exert anti-inflammatory effects. It provides a theoretical basis for research on the mechanism of galangin in treating AFLD and other diseases.

Meat products are an important part in our daily diet, providing valuable nutrients for the human body. However, heating processes cause the meat to become more appetizing with changes in texture, appearance, flavor, and chemical properties by the altering of protein structure and other ingredients. As one kind of cooking-induced contaminants, heterocyclic aromatic amines (HAAs) are widely present in protein aceous food products with strong carcinogenic and mutagenic properties. In order to promote the safety of traditional meat products, this review focused on the formation, metabolism, biological monitoring and inhibitory mechanism of HAA. An overview of the formation pathways, hazards, and control methods of HAAs during food processing in recent years was studied, aiming to provide some valuable information for exploring effective methods to inhibit the production of associated hazards during food processing. Systematic selection of different types of flavonoids to explore their effects on the formation of HAAs in an actual barbecue system can provide theoretical reference for effectively controlling the formation of HAAs and reducing their harm to human health.

The present study aimed at making a rational usage for European eel bone by-products by preparing Europen eel bone peptide chelated calcium (EBPC-Ca). Nutritional properties and bioactivity of EBPC-Ca were evaluated. Results showed that nutritional properties of calcium ions will cause intra- and inter-molecular folding and aggregation of peptide to uniformly form EBPC-Ca chelate. The chelated compound of EBPC and calcium ion triggered a strong apoptosis in heterogeneous human epithelial colorectal adenocarcinoma (Caco-2) in concentration- and time-dependent manners. Western blot analysis revealed that the EBPC-Ca induced apoptosis may be the result of a blocked autophagy flux through mitochondrial-dependent pathway. Additionally, the increase in FGF-23 protein expression inhibited the absorption of calcium ions and alleviated cell apoptosis. It was also found that the cell apoptosis occurs with significant increases in the levels of reactive oxygen species (ROS) and Ca²⁺ in the cells, indicating the anti-tumor potential of EBPC-Ca may involve multiple channels.

Dihydromyricetin (DHM), as a bioactive flavanonol compound, is mainly found in "Tengcha" (Ampelopsis grossedentata) cultivated in south of China. This study aimed to investigate the anti-hyperglycemic and anti-dyslipidemic activities of DHM using type 2 diabetes mellitus (T2D) rats, which was induced by feeding with high fat and fructose diet for 42 days and intraperitoneal administration of streptozocin. Forty-eight freshly-weaned rats were randomly assigned into the negative control (Blank), low dose (100 mg/kg), medium dose (200 mg/kg), high dose (400 mg/kg), and positive (40 mg/kg, met) groups. Fasting blood glucose and body weight were measured at weekly interval. Oral glucose tolerance tests were performed on days 42. The results revealed that DHM possessed significant antihyperglycaemic and antihyperinsulinemic effects. Moreover, after the DHM treatment, p-Akt and p-AMPK expression was upregulated, and glycogen synthase kinase-3β (GSK-3β) expression was downregulated, indicating that the potential anti-diabetic mechanism of DHM might be due to the regulation of the AMPK/Akt/GSK-3β signaling pathway.

The objective of this study was to investigate the effects of agar oligosaccharide-iron (AOS-iron) on intestinal tissue pathology and microbiota in IDA rats induced by a low-iron diet, further to find the relationship between intestinal microbiota and iron metabolic disorders. After 4 weeks of AOS-iron supplementation, the fecal iron content of IDA rats markedly increased in a dose-dependent manner, only the damaged cecum and colon tissues in medium-dose (MD) and high-dose (HD) groups were repaired to the baseline, while the diversity of gut microbiota was improved even at low dose (LD). Furthermore, the supplementation of AOS-iron altered the composition of gut microbiota. At the genus level, the beneficial microbiota was enriched in AOS-iron groups, but the relative abundance of potential opportunistic pathogens obviously reduced compared to that in the anemia model (AM) group. Spearman's correlation analysis revealed that biochemical parameters, including blood metabolic parameters, iron contents, body weight, GSH-PX and T-AOC activity, were positively correlated with SMB53, Anaerotruncus, Anaerostipes and Coprobacillus but negatively correlated with Morganella, Fusobacterium and Serratia. These findings indicated that AOS-iron effectively repaired the damaged intestinal tissue and ameliorated iron metabolic disorders by regulating gut microbiota desirably, which could provide references for the treatment of IDA.