Journal of Food Biochemistry最新文献

Based on the notable antibacterial and antioxidant functions of Eurotium cristatum, this study aims to evaluate the effects of its tea infusion resuspension on the storage quality of postharvest mango fruit, screen the optimal treatment concentration, and clarify the pathways of delaying postharvest senescence of mango by regulating the activity of reactive oxygen species (ROS) metabolic enzymes, thereby providing a theoretical basis and technical support for postharvest preservation of mango. Freshly harvested “Jin-Huang” (Mangifera indica) mangoes were divided into four groups: One was immersed in sterile distilled water for 30 s as control (CK), while the other three groups were immersed in E. cristatum tea infusion resuspensions at concentrations of 10% (v/v), 1% (v/v), and 0.1% (v/v), respectively. The efficacy of different treatments was evaluated by comprehensively assessing their impact on mango physiological indices after storage. Compared to CK, immersion in a 1% (v/v) E. cristatum resuspension yielded the most significant benefits after 9 days of storage. Fruits’ firmness increased by 1.90 kg·cm⁻², while decay rate and disease index decreased by 55.60% and 32.00%, respectively. The nutritional quality of the mangoes was also improved, with an increase in the contents of total flavonoids (0.28 mg·g⁻¹), total phenolics (0.81 mg·g⁻¹), titratable acidity (1.12%), cellulose (3.38 mg·g⁻¹), and ascorbic acid (0.04 μg·g⁻¹). Additionally, the activities of antioxidant enzymes increased by 27.86 U·mg⁻¹ for superoxide dismutase (SOD), 1.38 U·mg⁻¹ for peroxidase (POD), and 49.50 U·g⁻¹ for catalase (CAT). Concurrently, the accumulations of hydrogen peroxide (H₂O₂) and malondialdehyde (MDA) decreased by 0.37 μmol·g⁻¹ and 9.05 nmol·g⁻¹, respectively. In summary, treatment with a 1% (v/v) E. cristatum tea infusion effectively delayed the ripening and senescence of postharvest mangoes, significantly reducing decay and disease incidence while enhancing the antioxidant defense systems. These findings support the potential of E. cristatum as a natural preservative for mangoes and provide a theoretical basis for applications in other tropical fruits.

L. Corsi, N. Rubattu, S. Salis, et al., “In Vitro Proinflammatory and Cytotoxic Activity of Chicken-and Turkey-Based Würstels: A Preliminary Report,” Journal of Food Biochemistry 2024 (2024): 3229770, https://doi.org/10.1155/2024/3229770.

In the article titled “In Vitro Proinflammatory and Cytotoxic Activity of Chicken- and Turkey-Based Würstels: A Preliminary Report”, there was an error in Figure 4 related to the y-axis labels being presented in Italian instead of English. In addition, some information regarding the author contributions has also been omitted from the Title Page.

These errors were introduced during the production of the manuscript and should be corrected as follows:

We apologize for these errors.

RETRACTION: M. E. El-Beeh, M. Aljabri, H. F. Orabi, S. H. Qari, and M. F. Ramadan, “Ameliorative impact of cold-pressed Rosmarinus officinalis oil against liver toxicity and genotoxic effects in streptozotocin-induced diabetic rats and their offspring,” Journal of Food Biochemistry 43, no. 7 (2019), https://doi.org/10.1111/jfbc.12905.

The above article, published online on 20 May 2019 in Wiley Online Library (https://wileyonlinelibrary.com), has been retracted by agreement between the journal’s Editor-in-Chief Prisca-Maryla Henheik and Wiley Periodicals LLC. A third party reported that cell image sections had been duplicated between Figures 1(e) and 1(h) and that images of comet assays in Figure 2 showed evidence of manipulation. Additional investigation by the publisher found evidence of image manipulation and duplication in Figures 1(c), 1(d), 1(e), and 1(f) and that all images in Figure 2 showed evidence of cloning and insertion. The authors did not respond to an inquiry and request for original data by the publisher.

The retraction has been agreed because the evidence of image manipulation and fabrication fundamentally compromises the editors’ confidence in the results presented. The authors did not respond to the notice regarding the retraction.

This study aimed to investigate the anti–ovarian cancer activity of lotus seedpod polysaccharide (LSP) on human ovarian cancer SKOV3 cells and the relevant molecular mechanisms. The toxicity of LSP was also assessed in normal mice. The results showed that LSP inhibited SKOV3 proliferation and induced cell apoptosis. Transcriptomic and proteomic analyses indicated that LSP induced significant changes in gene and protein expressions, and their combined analysis showed necroptosis as one of the main pathways, which was confirmed by Hoechst 33342/PI double staining and western blot analysis. Moreover, LSPs significantly upregulated the protein expressions of RIPK1, phospho-RIPK1, RIPK3, phospho-RIPK3, MLKL, phospho-MLKL, TNFRSF1A, FTH1, and FTL. Meanwhile, LSP increased ΔΨm loss and the ROS level in SKOV3 cells. Furthermore, LSP showed no acute toxicity to normal mice in the dose range of 50–450 mg/kg·bw. These results suggest that LSP is a safe active ingredient that exerts anti–ovarian cancer activity in SKOV3 cells by inhibiting proliferation, inducing cell apoptosis, and inducing necroptosis via the RIPK1/RIPK3/MLKL pathway. These findings are helpful to the application of LSP in anti–ovarian cancer and the high-value utilization of lotus seedpod resources.

Folic acid (FA) is a water-soluble vitamin absorbed in the small intestine through the proton-coupled folate transporter (PCFT) when taken orally. In this study, we investigated the effect of green tea on PCFT-mediated FA transport. Green tea inhibited FA uptake by PCFT in a concentration-dependent manner, with an IC₅₀ value of 6.1%. When coincubated with 5% green tea, the K_m value of FA slightly increased, while the V_max value remained nearly unchanged. This suggests that green tea competitively inhibits the transport of folate through PCFT. When cells were pretreated with green tea or epigallocatechin gallate (EGCG), FA uptake by PCFT decreased in the absence of the inhibitor. This pretreatment showed minimal time-dependent effects while exhibiting concentration-dependent effects. FA uptake by PCFT was reduced after 10 min of pretreatment with green tea or EGCG and recovered in a time-dependent manner. EGCG stability was investigated, revealing that EGCG degrades at pH 7.4 but remains stable at pH 6.0, and the degradation at pH 7.4 was suppressed by the addition of ascorbic acid. These results indicate that EGCG was stable in inhibition experiments at pH 6.0 with green tea or EGCG and that the reduction in FA uptake observed after pretreatment with green tea or EGCG was most likely not due to EGCG.

Gastrodia elata Blume (GE) is recognized as a plant with both nutritional and medicinal properties, reported to exhibit neuroprotective and antioxidant effects, which contribute to its widespread use in various fields. However, the mechanisms underlying these effects remain insufficiently understood. In this study, we utilized ultrasound-assisted extraction to isolate water-soluble substances from GE and conducted in vitro antioxidant assays to evaluate the capacity of Gastrodia elata water extract (GWE) to scavenge DPPH and ABTS free radicals. Further investigation into the antioxidant and neuroprotective potential of GWE was conducted through in vivo studies using Caenorhabditis elegans (C. elegans). It was observed that GWE at concentrations of 50, 100, and 200 μg/mL enhanced locomotion and antistress capabilities while significantly reducing levels of H₂O₂, O₂⁻, lipofuscin, and reactive oxygen species (ROS). Concurrently, glutathione levels were significantly elevated. GWE supplementation stimulated the activity of serotonergic, dopaminergic, and GABAergic neurons, thereby improving locomotor abilities, including body bends, head thrashing, foraging behavior, and chemotaxis. Notably, significant increases in the relative concentrations of gamma-aminobutyric acid (GABA) and serotonin were also observed. Further research demonstrated that GWE treatment elevated the mRNA levels of genes associated with GABA and serotonin in the treated nematodes, specifically the unc-25, unc-46, unc-49, unc-47, tph-1, mod-1, mod-5, cat-4, cat-1, and exp-1 genes. Additionally, GWE treatment significantly enhanced the expression of the daf-16, sod-3, skn-1, hsf-1, and hsp-16.2 genes. GWE also promoted the translocation of DAF-16 into the nucleus, upregulated the expression of SOD-3::GFP, and downregulated the expression of gst-4 and GST-4::GFP. Spearman’s correlation analysis revealed a significant positive association between the daf-16, hsp-16.2, cat-1, unc-46, unc-47, and mod-1 genes and the levels of serotonin, GABA, and locomotor behaviors. This study enhances our understanding of the mechanisms through which GWE exhibits neuroprotective and antioxidant properties, thereby elucidating the health benefits of GE for living organisms.

Myocardial fibrosis (MF) is a major contributor to cardiovascular dysfunction and remains a key target for therapeutic intervention. Cordyceps sinensis, also known by its updated taxonomic name Ophiocordyceps sinensis, is traditionally recognized in the form of a fungus–insect complex and has long been regarded as a functional food with therapeutic benefits for renal and pulmonary health. However, its potential effects on MF remain poorly understood. Owing to the scarcity and high cost of wild O. sinensis, fermented cordyceps powder (FCP), a standardized mycelial fermentation product derived from symbiotic microorganism associated with O. sinensis, has gained attention as a promising and accessible alternative in pharmacological research. Given the pharmacological similarity between O. sinensis and FCP, we first applied network pharmacology to identify potential therapeutic targets of O. sinensis representative bioactive compounds. Protein–protein interaction (PPI) network construction and functional enrichment analysis revealed associations with collagen regulation and amino acid metabolism. These predictions were validated in vivo through FCP administration and metabolomic analysis. Using an isoproterenol (ISO)-induced MF rat model, we demonstrated that FCP significantly attenuated MF, as evidenced by markedly reduced collagen deposition (Masson’s trichrome staining), hydroxyproline levels, and collagen I expression. UPLC-MS metabolomics revealed that FCP modulated amino acid metabolic pathways, particularly glycine, serine, and proline metabolism. Mechanistically, FCP exerted its effects by downregulating key components of the TGF-β1/Smad pathway, including TGF-β1, Smad4, and p-Smad2/3, while increasing the inhibitory Smad7 expression. This dual modulation of signaling and metabolism suggests that FCP has antifibrotic potential and may serve as a functional food-derived intervention against cardiovascular fibrosis.

B. Li, J. Li, and S. Hu, “Cinnamon could improve hepatic steatosis caused by a high-fat diet via enhancing hepatic beta-oxidation and inhibiting hepatic lipogenesis, oxidative damage, and inflammation in male rats,” Journal of Food Biochemistry 2022 (2022): e14077, https://doi.org/10.1111/jfbc.14077.

The article titled “Cinnamon could improve hepatic steatosis caused by a high-fat diet via enhancing hepatic beta-oxidation and inhibiting hepatic lipogenesis, oxidative damage, and inflammation in male rats” has inadvertently been assigned to a Special Issue due to a Publisher error. The article should have been published within the regular issue of Journal of Food Biochemistry.

We apologize for this error.

Postbiotics derived from probiotic components or metabolites have emerged as promising therapeutic agents for managing inflammation and oxidative stress–related diseases. The inhibitory effects of the peptidoglycan (PGN) fraction of Bifidobacterium animalis KL101 on receptor activator of nuclear factor–kappa B (NF-κB) ligand (RANKL)–induced osteoclast differentiation were investigated in RAW264.7 macrophages. PGN (10 and 20 μg/mL) significantly reduced tartrate-resistant acid phosphatase (TRAP) activity, suppressed nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), and downregulated osteoclast-specific genes such as matrix metalloproteinase-9 (MMP-9) and Cathepsin K (CtsK). Moreover, PGN decreased intracellular reactive oxygen species (ROS) levels and upregulated heme oxygenase–1 (HO-1), mitigating ROS-mediated signaling pathways such as the NF-κB pathway. In addition, PGN also modulated autophagy, reducing the ratio of microtubule-associated protein 1 light chain 3–II to LC3–I (LC3–II/LC3–I) and restoring p62/SQSTM1 (p62) levels, thereby impairing osteoclastogenesis. These findings highlight the dual role of PGN from B. animalis KL101 in inhibiting ROS and autophagy pathways critical to osteoclast differentiation and function. This study identifies the PGN of B. animalis KL101 as a promising postbiotic candidate for controlling osteoclast-mediated bone degradation in disorders such as osteoporosis and periodontitis.

Vitamin D deficiency is linked to various chronic diseases, including obesity, insulin resistance, hyperlipidemia, liver disease, and hypertension. This study investigates the comparative effects of vitamin D3 supplementation and sunlight exposure on high-fat diet–induced obesity in albino mice. After 16 weeks on a butter-rich diet, obese mice gained 15 ± 2 g more than controls (T₀). The obese cohort was then subdivided into four groups (8 mice each): untreated obese controls (T₁), sunlight exposure (T₂), vitamin D₃ supplementation (T₃), and combined sunlight plus vitamin D₃ supplementation (T₄). After 30 days, the obese control group exhibited significant weight gain with elevated glucose, cholesterol, triglycerides, LDL, and liver enzymes, alongside reduced HDL levels (p < 0.001). In contrast, all treatment groups, particularly those receiving combined sunlight and vitamin D₃, showed marked improvements in these parameters, including significant reductions in metabolic markers and liver enzymes (p < 0.001). Serum 25 (OH) D levels remained stable in normal controls (30–32 ng/mL), declined in obese controls (15–18 ng/mL), increased moderately with sunlight (33–35 ng/mL) or synthetic vitamin D₃ (32–34 ng/mL), and reached the highest values under combined treatment (37–39 ng/mL). Histological analysis revealed fat accumulation in the liver and kidneys, as well as adipocyte infiltration in the liver and heart of obese controls, changes not observed in treated groups. Collectively, these results indicate that improving vitamin D status via sunlight exposure or supplementation may offer a simple and effective approach to alleviating obesity-related metabolic dysfunction.