Journal of Food Biochemistry最新文献

Atopic dermatitis (AD) is a chronic inflammatory skin disorder requiring continuous care and treatment. Therefore, exploring the therapeutic potential of natural ingredients for AD is essential. This study conducted a network analysis to investigate the anti-AD effects of propolis and its underlying mechanism, with a focus on the compositional differences between Korean and Brazilian propolis. To identify the bioactive components and related mechanisms, differentially expressed genes (DEGs) in AD-induced HaCaT cells with and without propolis treatment were identified. NCBI, SwissTargetPrediction, STITCH, and the Comparative Toxicogenomics Database (CTD) were used to identify target genes of the propolis compounds, and these genes were compared with the DEGs to identify the shared target genes. Notably, CXCL10 and CCL2 were highly associated with target genes shared between Korean and Brazilian propolis, with Korean propolis affecting TLR4, RIPK2, and PYCARD and Brazilian propolis influencing CEBPB, PTGS2, and DAB2IP. Korean propolis was found to predominantly impact the regulation of mast cell activation and the cytosolic DNA-sensing pathway, whereas Brazilian propolis primarily affects Type I interferon–mediated regulation and the TNF signaling pathway. Additionally, both the TNF and IL-17 signaling pathways were implicated in the mechanisms of both Brazilian propolis and Korean propolis. Furthermore, our study validated the therapeutic potential of propolis in AD treatment, as evidenced by significant reductions in TNF-α, IFN-γ, IL-4, IL-13, CXCL10, CCL2, and histamine release in an AD-induced model. This study confirms the efficacy of Korean and Brazilian propolis in treating AD and reveals molecular mechanism differences due to variations in major components and target genes.

Browning reactions caused by oxidative stress occurring during postharvest procedures significantly compromise the quality of ready-to-eat (RTE) vegetables, negatively affecting their market value. Polyphenol oxidase (PPO) and peroxidase (POD) are two major enzymes involved in this phenomenon, as they oxidize phenolic compounds to quinones, which in turn polymerize to brown pigments. Recently, there has been an increasing interest in developing antibrowning treatments using food by-products. Herein, the efficiency of a kiwi peel extract in reducing enzymatic browning of minimally processed lettuce (Lactuca sativa) has been investigated. PPO and POD activities showed an opposite spatial distribution within the leaf, with a higher POD activity in the midvein (MV) and in the inner lamina tissues, and a prevalence of PPO activity in the mesophyll. Considering that MV lignified tissues are those mainly affected by browning, the temporal trend of POD activity over a 20-day storage period at 4°C was investigated. Data showed that treatment with a kiwi peel extract hinders both the increasing trend of POD activity and browning development compared to control leaves. These results could be potentially useful for the industry as they confirm that natural extracts, such as kiwi peel extract, can be valuable for extending the shelf-life of RTE products.

Cholangiocarcinoma (CCA) is a very aggressive cancer and CCA treatments with cisplatin and 5-fluorouracil (5-FU) often cause side effects and drug resistance. This study aimed to investigate the combined effects of Valencia KK4-type peanut’s (Arachis hypogaea L.) skin ethanolic extract (KK4-PSE) and cisplatin or 5-FU on CCA cells in vitro and in nude mouse xenografts. Antiproliferative activity was evaluated using MTT assay. The in vitro drug interaction was studied by the Chou–Talalay method. Apoptosis induction and cell cycle arrest were analyzed by flow cytometry. The levels of proteins involved in apoptosis were evaluated by western blot analysis. Mouse xenograft models were used to evaluate the anticancer activity of KK4-PSE in animals (in vivo). KK4-PSE inhibited the proliferation of CCA cell line (IC₅₀ = 37.22 ± 4.31, 26.27 ± 0.78, and 17.72 ± 0.50 μg/mL at 24 h, 48 h, and 72 h exposures, respectively) more effectively than that of the noncancer H69 cholangiocyte cell line (IC₅₀ = 193.35 ± 6.55, 75.35 ± 1.00, and 57.41 ± 0.96 μg/mL at 24 h, 48 h, and 72 h exposures, respectively). In KKU-M213B cells, KK4-PSE treatments in combination with cisplatin caused cell cycle arrest at G2/M, whereas combined KK4-PSE and 5-FU caused a significant increase of Sub G1 population for 24 h exposure. Furthermore, a significant increase in the percentage of apoptotic cells was also observed in combination treatments. The combination treatments of KK4-PSE with cisplatin and 5-FU caused downregulation of pERK1/2 and Bcl2 and caused a decrease in the Bcl2/Bax ratio, resulting in enhanced apoptosis. In addition, KK4-PSE treatments in combination with 5-FU suppressed tumor growth in BALB/cAJcl-Nu/Nu xenograft models more effectively than the combinations with cisplatin. Taken together, KK4-PSE may be an effective synergistic agent with 5-FU and cisplatin for CCA chemotherapy, warranting further clinical examination.

The study delved into the rate of browning (A₄₂₀ nm) within a model wine solution, aiming to elucidate mechanisms impacting real product scenarios, including low- and no-alcohol wines. The model wine solutions were prepared by adding tartaric acid, caffeic acid, and catechin into an aqueous ethanol solution containing transition metals (iron [Fe] and copper [Cu]) along with sulfur dioxide (SO₂). The results indicated that the model wines without ethanol exhibited the highest browning rates both in the presence (k = 0.0022 day⁻¹) and absence (k = 0.0035 day⁻¹) of SO₂. Notably, ethanol concentration showed a negative correlation with kinetic rates in both scenarios: with SO₂ (r = −0.9317) and without SO₂ (r = −0.9667). The addition of Fe and Cu separately led to a slight elevation in browning, particularly evident with Fe, while adding only Cu exhibited nonsignificant impact. However, their combined addition revealed a marked synergistic effect, rendering the rate notably sensitive to Cu concentration.

Background: Protein instability has been reported to be an important cause of haze in white wines; to investigate the feasibility of protease as a substitute for bentonite in the protein stability of white grape liqueurs, the effect of protease combined with heat treatment on the composition and protein stability of liqueur wines was investigated by chemical analysis, sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE), and amino acid analysis.

Results: The results showed that the contents of total acid, volatile acid, pH, and glycerol were not significantly different from the blank control; the effect on total protein content and thermal stability were similar to the bentonite treatment; the L^∗, b^∗, and $$ values of liqueur wines increased by 5.59%, 4.33%, and 4.33% after protease combined with heat treatment (p < 0.05); SDS-PAGE results confirmed that protease combined with heat treatment had good hydrolysis for thaumatin-like proteins (TLPs) and chitinases (CHIs) in liqueur wines. Amino acid analysis revealed that the levels of threonine, serine, tyrosine, arginine, and proline had increased, respectively, and isoleucine (1.26 mg/L) and leucine (1.16 mg/L) were newly detected after protease combined with heat treatment. Particle size analysis showed that the protease combined with heat treatment had less effect on the particle size distribution of the wines.

Conclusion: Protease combined with heat treatment had a certain protein stabilizing effect and had no significant negative impact on other nutrients of liqueur wines. Thus, it can be used as an alternative to bentonite for the protein stabilization of liqueur wines.

Background: Renal involvement resulting from hyperuricemia, known as hyperuricemia nephropathy (HN), is characterized by chronic tubulointerstitial inflammation caused by extensive urate crystal deposition. Managing this condition requires straightforward preventive or therapeutic interventions, primarily through dietary measures.

Methods: In this study, the mouse model of HN was established using yeast extract combined with potassium oxonate. The effect and potential mechanism of β-sitosterol in treating HN were investigated through biochemical indexes, pathological changes, untargeted metabolomics, and network pharmacology.

Results: β-Sitosterol reduced the levels of four biomarkers of HN: uric acid (UA), creatinine (CRE), blood urea nitrogen (BUN), and xanthine oxidase (XOD). It also mitigated inflammatory injury in renal tissues and reversed the abnormal expression of four key urate transporter proteins: glucose transporter protein 9 (GLUT9), organic anion transporter 1 (OAT1), ATP-binding cassette transporter G2 (ABCG2), and urate transporter 1 (URAT1). To explore the mechanism of β-sitosterol in treating HN, this study employed network pharmacology and metabolomics to analyze 27 intersecting gene targets and 14 differential metabolites. The findings indicated that glutathione (GSH) metabolism might be a crucial pathway. Treatment with β-sitosterol increased the levels of reduced GSH as well as the activity and expression of 6-phosphogluconate dehydrogenase (G6PDH) in mice, thereby effectively modulating GSH metabolism. This study proposes a novel strategy using β-sitosterol for treating HN, providing a promising approach for addressing this condition.

Apple is a perishable fruit due to its higher moisture content, which leads to spoilage and also reduces its shelf life. To improve the storage stability of apples, drying is the most effective and oldest method as it leads to the reduction of water activity. In the present study, dried apple slices were developed from “Golden Delicious” apples. The suggested methodology involves the use of dried apple slices with skin and a thickness of 4.5 mm, pretreated with 1% salt solution for 15 min. The drying process takes place at a temperature of 50°C for 3 h, followed by a temperature of 90°C for 2 h. The water activity of salt- and KMS-pretreated dried apple slices was 0.422 ± 0.00 and 0.438 ± 0.01, respectively, whereas a higher value 0.473 ± 0.01 of water activity was observed in untreated dried apple slices, demonstrating better stability. Also, compared to the control sample, the pretreated slices showed 13% lesser shrinkage due to drying, thereby retaining its shape. The total phenolic content was the lowest in the control sample (101.52 ± 0.37 mg GAE/100 g), while a significant increase was observed in KMS-pretreated (115.44 ± 4.08 mg/100 g) and salt-pretreated (131.55 ± 0.58 mg/100 g) dried apple slices. Moreover, antioxidant activity also was higher in salt-pretreated dried apple slices. Texture profile analysis revealed that the developed apple slices had better crispiness than nonpretreated ones. Thus, pretreatment before drying is of great significance to improve the appearance and quality of products.

Acclimation refers to the process by which plants adapt to the environment. This study was to illustrate the effect of acclimation length on the metabolic profile of tea leaves. In this study, 32 long-acclimated tea varieties in Shandong Province and 61 ST varieties were used as materials, and the metabolites of tea plants were detected by using UPLC-MS/MS method. The results showed that the accumulation of flavonoids, organic acids, and alkaloids in long-acclimated tea plants was higher than that in ST plants. In contrast, the accumulation of phenolic acids, lipids, and amino acids showed an opposite trend. In long-acclimated tea varieties, Camellia sinensis cv. Lucha11 (LC11), LC24, and LC30 showed high flavonoids, phenolic acids, organic acids, and alkaloids, which were important metabolites and related to tea quality. This study provides a theoretical basis for understanding the effect of environment on metabolism of tea plants and guides the breeding of new tea varieties with high quality or special flavor.

Purpose: Pulmonary arterial hypertension (PAH) is a fatal condition characterized by poor control of pulmonary hemodynamics and vascular development. Zang Siwei Qingfei mixture (ZSQM) is a traditional Chinese medicine formula used for the treatment of chronic respiratory diseases. However, the underlying mechanism of ZSQM for treating PAH remains unclear.

Methods: A PAH rat model was established after monocrotaline (MCT) injection, and pulmonary hemodynamic features and pathological changes were evaluated. The candidate targets of ZSQM against PAH were discovered using network pharmacology. Then, molecular docking was used to validate the discovered key targets. Moreover, serum metabolomics was used to identify differential metabolites. The metabolomics and network pharmacology integrated network was constructed.

Results: ZSQM alleviated MCT-induced pulmonary vascular injury and vascular remodeling. We found ZSQM core component chrysin and six hub genes according to network pharmacology, including CYP2C19, CASP8, PTK2, VEGFA, FLT4, and TNNI3. Molecular docking revealed strong binding affinities between key targets and chrysin. Meanwhile, western blotting results validated significant changes in the expression of these key targets. Subsequently, we confirmed that chrysin existed in the ZSQM by HPLC–MS. In addition, a total of 19 metabolites with potential significance were identified to be implicated in the therapeutic mechanisms of ZSQM. The further integrated analysis indicated an interconnection between these key targets, their related core metabolites (12(S)HETE, ascorbate, succinate, vitamin C, and L-arginine), and metabolic pathways.

Conclusion: The study, employing metabolomics and network pharmacology, has concluded that ZSQM has the potential to enhance the treatment of PAH by targeting multiple pathways and molecular targets. This finding suggests that ZSQM could serve as a promising alternative therapy for PAH.

In neurodegenerative diseases, the activation of microglia and the ensuing neuroinflammation are pivotal in regulating disease progression. Attenuating inflammation induced by microglial cells is considered a key strategy for slowing the progression of neurodegenerative diseases. γ-glutamylcysteine (γ-GC) has exhibited significant antioxidative and anti-inflammatory effects; nevertheless, its potential role in modulating neuroinflammatory responses remains incompletely explored. The current investigation aimed to establish a neuroinflammation model by stimulating BV2 microglia cells with lipopolysaccharide (LPS) and to explore the protective effect of γ-GC on neuroinflammation in BV2 microglia cells. The results demonstrated that γ-GC significantly attenuated LPS-induced oxidative damage in BV2 cells, reduced the levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), inhibited the cytoplasmic translocation of high-mobility group box 1 protein (HMGB1), and effectively mitigated the LPS-induced inflammatory response in BV2 cells. We further investigated the regulatory mechanism of γ-GC on LPS-induced BV2 neuroinflammation and found that γ-GC significantly enhances autophagy in BV2 cells, resulting in a marked reduction in mammalian target of rapamycin (mTOR) phosphorylation levels and an increase in AMP-activated protein kinase (AMPK) phosphorylation levels. The use of autophagy inhibitors 3-methyladenine (3-MA) and AMPK inhibitors further corroborates the proposition that γ-GC promotes autophagy in BV2 cells while suppressing the LPS-induced inflammatory response of BV2 microglia through the activation of the AMPK-mTOR pathway. The findings indicate that γ-GC exerts a substantial inhibitory impact on neuroinflammation, making it a promising candidate for the development of therapeutic strategies against neuroinflammatory disorders and related conditions.