In this study, we investigated the ability of κ ‐carrageenan to reinforce the heat‐induced EWP/Car gel system. A series of composite gels containing 0%–1.0% κ ‐carrageenan was prepared and characterized. The results showed that moderate κ ‐carrageenan addition (particularly 0.6%) significantly improved gel hardness, elasticity, and water‐holding capacity. Rheological and microstructural analyses confirmed that κ ‐carrageenan promoted the formation of a denser, more homogeneous network, as evidenced by lower tan δ values and uniform fluorescence and pore distribution in CLSM and SEM images. FTIR and SDS‐PAGE results indicated that these enhancements were mediated by noncovalent interactions without altering protein secondary structures. Moreover, the reduction in free sulfhydryl groups and increased disulfide bond formation revealed a strengthened protein matrix. These findings provide promising insights for the rational design and application of EWP‐based systems in the production and processing of egg‐based food products.

CS is an environmental pollutant everywhere, but we still do not fully know how it hurts our skin. This study integrates LC-MS, network toxicology, molecular docking, and experimental validation in order to understand how CS causes skin involvement at the molecular level. By searching a database, constructing a PPI network and analyzing GO/KEGG, we found 57 candidate targets related to CS-induced skin damage. We found that STAT3, AKT1, TP53, CASP3 and IL-6 play the core roles, and PI3K-Akt, p53, JAK-STAT and apoptosis pathways may be crucial. Molecular docking analysis confirmed strong interactions between components of CS and these key targets. In vitro validation using HaCaT cells showed that CS exposure decreased expressions of STAT3 and AKT, but increased p53, CASP3 and IL-6. The inhibition of PI3K-AKT- and JAK-STAT-related responses, coupled with the initiation of p53-driven apoptosis, led to the observed cytotoxicity, functional impairment, oxidative stress and inflammation, which induced and aggravated skin damage. These findings provide a new perspective on the harmful effects of CS on the skin, providing both a theoretical basis for strengthening regulatory measures to limit exposure and opening new avenues for exploring relevant prevention strategies.

The medicinal plant Phyllanthus emblica Linn. has been recognized for its health‐beneficial properties and has a long history of cultivation in ancient China and India. However, its effects and main mechanism in high‐fat diet (HFD)‐induced metabolic syndrome (MetS) have not been revealed yet. According to our findings, emblica fruit powder (EFP) through the freeze‐drying process was able to modulate the composition of the intestinal microbiota, with a significant increase in the beneficial bacteria genera Lactobacillus and Turicibacter. In addition, fecal metabolite profiling revealed that 20 metabolites were deferentially expressed, which were mainly organic acids, amino acids, and their derivatives. They are primarily enriched in the biological process of lipid metabolism, including the metabolism process of cholic acid, glycerophospholipid, and α‐linoleic acid. Subsequent qPCR testing of the liver tissue suggested that the regulatory effects of EFP in HFD mice may stem from its influence on the expression levels of over 20 key genes involved in host metabolic processes. In conclusion, EFP is able to alleviate the MetS caused by HFD, and this positive impact may be partially through the regulation of the “gut‐liver axis.” Consequently, EFP holds potential as a functional food ingredient for the prevention and management of MetS.