Journal of Future Foods
·
2025
·
IF 7.2
Lei Dou,Zimu Zhang,Xiufang Huang,Yaobing Chen,Kai Luo,Jianquan Kan
Considering that the peptide from Idesia polycarpa Maxim.cake meal polypeptide (CIP) is a novel antioxidant agent, this study aimed to develop an efficient and safe food film by incorporating the CIP agent into a gelatin matrix. The films with different concentrations of CIP were characterised and applied in the preservation of nectarines. The results indicated that the CIPF/3% fraction exhibited significant moisture barrier properties, with a water vapor permeability (WVP) of only 8.12 % ± 0.09 %. Additionally, it demonstrated excellent mechanical and antioxidant properties, with scavenging capacities of 76.31 % ± 0.597 %, 65.98 % ± 0.444 %, and 60.98 % ± 0.231% for DPPH, ABTS, and hydroxyl radicals, respectively, surpassing those of other fractions. In nectarine freshness preservation, the Coating/3% fraction showed the best performance. It significantly reduced the weight loss rate of nectarines, improved fruit firmness, maintained the pH value, and minimized nutrient losses, including ascorbic acid and Total soluble sugars (TSS). Furthermore, it effectively preserved the bright surface color of nectarines and extended their shelf life. In summary, the specific environmental protection, safety, and preservation qualities of the CIPF/Coating in food packaging suggest a promising potential for its application.
研究领域:
食品科学
·
高分子科学
·
抗氧化技术
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食品保鲜
·
材料表征
·
可食用涂层
·
农业副产物利用
✓ 已验证
产品关联
DOI
高影响因子
Foods
·
2026
·Vol. 15
·期 10
·1740
·
IF 6
Xiufang Huang,Yifan Shi,Yaobing Chen,Jianquan Kan,Kai Luo
This study aims to improve the utilization ofIdesia polycarpacrude oil (IPCO) in the food industry by developing high-internal-phase emulsions (HIPEs) stabilized through ternary complexes (ovalbumin (OVA), xanthan gum (XG), and tannic acid (TA)). IPCO is highly prone to oxidation due to its polyunsaturated fatty acid (PUFA) content. Optimal formulations were obtained by varying the component concentrations and assessing the structure, stability, and fat-substitution potential. Under conditions of 0.6%w/vXG and 2.5%w/vOVA-TA, HIPEs exhibited a smaller particle size (3.31 μm), high centrifugal oil retention (99.29%), strong emulsifying activity (49.91 m2/g), and excellent stability (99.69%). Additionally, a formulation with 1.5%w/vOVA-TA and 0.8%w/vXG showed good wettability, particle size, and stability, possibly due to excessive self-aggregation of XG, which caused a decrease in emulsion stability and wettability. Structural analysis (FTIR, XRD, SEM, CLSM) revealed that the stability of the emulsions was mainly attributed to strong non-covalent interactions and a dense interfacial adsorption layer. In cookie applications, substituting 25%w/wbutter or 50%w/wshortening with HIPEs resulted in comparable texture to the control group. GC–MS analysis of relative fatty acid composition showed that partial replacement with IPCO-based HIPEs shifted the final biscuits toward a lower relative proportion of palmitic acid (C16:0) and a higher relative proportion of linoleic acid (C18:2n6c). Overall, OVA–TA–XG-stabilized HIPEs effectively delayed the oxidation of IPCO and enabled partial replacement of conventional solid fats in biscuits, thereby shifting the relative fatty acid composition of the final products toward a higher proportion of unsaturated fatty acids.
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DOI
PubMed
高影响因子
Food Science & Nutrition
·
2026
·Vol. 14
·期 4
·e71702
·
IF 5
Weijie Chang,Yaobing Chen,Jianquan Kan,Xiufang Huang,Kai Luo
While mounting evidence points to a potential link between industrial aluminum exposure and neurodegenerative diseases like Alzheimer's disease (AD), the precise intervention strategies remain an area of active research. This study proposes a “multi‐target synergy and dose threshold control” exploratory framework for evaluating Idesia polycarpa crude oil (IPCO) in an aluminum‐induced AD model. An integrated analytical approach employing GC–MS and network pharmacology was used to identify three candidate core components—(Z,Z)‐9,12‐octadecadienoic acid, Beta‐amyrin, and 2,4‐di‐tert‐butylphenol—that were computationally predicted to influence a network of 35 ad ‐related pathways (e.g., Calcium and PPAR signaling) via eight potential key targets (including PTGS2 , PPARG , and AKT1 ). In vivo experiments revealed a dose‐dependent modulation of AD‐related pathology following IPCO intervention. The high‐dose group showed the most marked improvements in several therapeutic markers, including reduced aluminum load, an anti‐inflammatory shift in cytokine levels (elevated IL‐10, decreased IL‐4, IL‐6, IL‐1β, and TNF‐α), and remodeling of the gut microbiota characterized by an increase in putative short‐chain fatty acid (SCFA)‐producing genera such as the [Eubacterium]‐xylanophilum‐group and NK4A214‐group ( Firmicutes ). Paradoxically, this same high dose was associated with a decline in spatial cognitive performance. This biphasic effect may be preliminarily explained by a dual microbial mechanism: the inhibition of the pro‐inflammatory associated [Eubacterium]‐oxidoreducens‐group alongside the expansion of taxa linked to a neuroprotective SCFA metabolic network. As one of the first studies to map these multi‐dimensional “constituent–microbiota–neuroinflammation” interactions for IPCO, our findings highlight its complex, dose‐sensitive bioactivity. Importantly, they underscore the critical need for subsequent pharmacokinetic and direct target engagement studies. Step 1: Component identification and target screening: The chemical composition of IPCO was characterized using GC–MS, identifying two major fatty acids and six fat‐soluble active substances. A total of 149 potential drug targets were predicted via Pharm Mapper and SwissTargetPrediction. Concurrently, 2029 genes associated with Alzheimer's Disease (AD) were retrieved from the OMIM, TTD, and GeneCards databases. Through the intersection analysis of “ingredient‐target‐disease,” combined with STRING‐based Protein–Protein Interaction (PPI) analysis, Gene Ontology (GO), and KEGG pathway enrichment, the molecular mechanisms underlying the neuroprotective effects of IPCO were elucidated. Step 2: Structural validation (molecular docking): Molecular docking simulations were performed to evaluate the binding affinity between active ingredients and core targets. The results demonstrated that the core component, β‐amyrin, exhibited high binding affinity with key protein targets. Specifically, the binding energies of β‐amyrin with PPARG and ERBB2 were −8.80 and −9.10 kcal/mol, respectively. These high‐affinity interactions provide structural evidence validating the predictions made through network pharmacology. Step 3: In vivo verification (gut microbiota and biochemical markers): In vivo experiments confirmed that IPCO intervention significantly modulated the gut microbiota in AD rats, notably increasing the abundance of the [Eubacterium]‐oxidoreducens‐group . Biochemically, IPCO treatment markedly enhanced the levels of SCFAs and the anti‐inflammatory cytokine IL‐10. Furthermore, a significant reduction in hippocampal Al accumulation and inhibition of AChE activity were observed. These findings suggest that IPCO exerts its anti‐AD effects potentially by modulating the gut‐microbiota‐brain axis and improving cholinergic system function. This study systematically elucidated the neuroprotective mechanisms of IPCO against AD through an integrated approach of network pharmacology, molecular docking, and in vivo experiments. Initially, eight core active ingredients were identified in IPCO via GC–MS, with 149 potential targets and 2029 ad ‐related genes mapped through multi‐database screening. Molecular docking further validated that the core component, β‐amyrin, exhibited high binding affinities for key targets including PPARG (−8.80 kcal/mol) and ERBB2 (−9.10 kcal/mol). Finally, in vivo verification demonstrated that IPCO intervention significantly modulated the gut‐microbiota‐brain axis by increasing the abundance of the [Eubacterium]‐oxidoreducens‐group , elevating levels of SCFAs and IL‐10, while concurrently reducing hippocampal Al accumulation and inhibiting AChE activity.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）