Journal of Food Biochemistry最新文献

It is of great significance to develop natural active substances for treating Alzheimer’s disease (AD). We constructed an AD cell model using Aβ₂₅₋₃₅-induced PC12 cells to assess isolated components from Tibet wild Gymnadenia crassinervis protective and reparative effects against Aβ₂₅₋₃₅-induced cell injury. The results indicated that the active fraction extracted and isolated from Gymnadenia crassinervis strongly inhibited acetylcholinesterase (AChE) with an excellent IC₅₀ value as low as 135.86 ± 5.59 μg/mL. The main compound of the Gymnadenia crassinervis active fraction was preliminarily identified as dactylorhin A by LC-MS. The high-concentration group, treated with 10 μg/mL of the Gymnadenia crassinervis active fraction, exhibited significantly protective effects, the treatment of which enhanced cell viability and mitigated cell shrinking induced by Aβ₂₅₋₃₅. The ROS level and MDA content in the high-concentration group cells decreased by approximately 28% and 30%, respectively, while the activities of SOD and CAT even increased by about 92% and 221%, respectively. In addition, Western blotting analysis showed that the Gymnadenia crassinervis active fraction inhibited apoptosis. Therefore, these findings suggest that the Gymnadenia crassinervis active fraction can repair Aβ₂₅₋₃₅-induced cell injury, protect against Aβ toxicity, and hold potential in both preventive and therapeutic aspects of AD.

Ferulic acid (FA) is a common phenolic acid in plants and is known to effectively combat cancer; however, the precise mechanism is still unknown. In this study, we examined the effect of FA on breast cancer (BC) cells, together with its molecular mechanism. We observed that FA greatly decreased BC cell viability without any obvious inhibitory effects on normal cell viability. Further, FA could significantly lead to the apoptosis of MDA-MB-231 cells. FA administration dramatically increased the levels of reactive oxygen species (ROS) in MDA-MB-231 cells, and mitochondria-dependent apoptosis occurred via the MAPK/STAT3/NF-κB pathways. It was also demonstrated that with an increase in FA treatment time, the G2/M phase ratio increased and the expression of p-AKT and cycle-related proteins was inhibited. The migration of MDA-MB-231 cells was significantly inhibited after FA treatment. FA reduced N-cadherin, vimentin, and SNAI 1 expression levels through the MAPK signaling pathway. Pretreatment with N-acetylcysteine and MAPK inhibitors (SP600125 or SB203580) increased the expression of these proteins, whereas pretreatment with the MAPK inhibitor (FR180204) decreased their expression. In conclusion, FA can increase ROS levels, induce mitochondria-dependent apoptosis, block the G2/M phase cycle, and inhibit cell migration. Thus, FA may be a promising new medication in the treatment of BC.

The emergence and spread of methicillin-resistant Staphylococcus aureus (MRSA) is a major cause of bacterial infections in healthcare. Lysostaphin, a Zn²⁺-dependent endopeptidase, hydrolyzes the glycine (G)-linked pentapeptide bridge in the pathogen Staphylococcus aureus. In this study, the stability of lysostaphin was improved by engineering the addition of disulfide bonds around the protein’s Zn²⁺ binding site through molecular dynamics simulation. Further mutagenesis to add polyG at the C-terminus yielded combination variant 319/252-G₃, which was 2.6-fold more stable than lysostaphin after 30 min at 60°C. Optimization of the C-terminal glycine number produced variant 319/252-G₆, which retained 67.3% of its antimicrobial activity after 30 min at 70°C, and could be resistant to milk pasteurization conditions. Based on this, a probiotic strain of Escherichia coli Nissle 1917 to constitutively express and secrete lysostaphin from a mutated lac operator was engineered, resulting in effective control and prevention of S. aureus contamination in milk. One possible biotechnological application to utilize lysostaphin and probiotic strains can be used in animal feed and food additives for the prevention and treatment of S. aureus infections.

Ultraprocessed foods represent a severe concern to human health due to their direct link with metabolic diseases. Among these foods, mechanically separated meat-based products are of particular interest due to the use of preservatives and the possible presence of antibiotic residues free or bound to animals’ bone fragments. To demonstrate the potential harmfulness of these substances, 28 samples of commercially available würstels of different suppliers, price category, package size, and produced with mechanically separated chicken and turkey meat were randomly collected from the Italian market. The presence of antibiotics was assessed by LC/HRMS; bone fragments were identified using histological, histochemical, and microscopical analyses; the cytotoxic and proinflammatory activity of the würstels and their ingredients was assessed using ELISA. Bone fragments were detected in all samples, while only 9 out of 28 samples were positive for the presence of doxycycline, although at concentrations far from the maximum residue limits, ranging from 0.36 to 2.50 ug/kg. Most of the samples were cytotoxic at a dilution of 1 : 20 while all of the 3 tested exerted a proinflammatory effect, with significant cytokines’ release (IL-1α, IL-1β, IL-6, IL-8, INF-γ, TNF-α, GM-CSF, and MCAF) at 24 and 36 h ( ^∗∗∗P < 0.001). Part of the cytokine release was due to the presence of beech- and oak-based smoke flavoring, where a significant release of IL-1β ( ^∗∗∗P < 0.001), IL-8 ( ^∗∗∗P < 0.001,  ^∗∗P < 0.01), INF-γ ( ^∗P < 0.05 and  ^∗∗P < 0.01), and MCAF ( ^∗∗∗P < 0.001) was observed at 12 and/or 24 h. Although the results need further investigation to elucidate the cytotoxic and proinflammatory process, this can be considered one of the first reports shedding light on the possible toxic potential of some substances routinely used in food processing, even at allowed concentrations. Moreover, it provides new insights into the understanding of the link between high consumption of ultraprocessed meat, increased risk of inflammation, and progression of chronic diseases.

Background. Kaempferol is a natural flavonoid with a wide range of pharmacological effects. The current study tested whether kaempferol prevents hypertension-induced renal remodelling in rats. During the 5 weeks of experiments, rats (n = 7/group) were administered N_ω-nitro-L-arginine methyl ester hydrochloride (L-NAME) (40 mg/kg/day) with either vehicle or kaempferol (20 mg/kg/day) or kaempferol (40 mg/kg/day) or lisinopril (5 mg/kg/day). Results. Kaempferol treatment alleviated haemodynamic changes occurring in hypertensive rats, including increases in systolic and diastolic blood pressure, pulse pressure, mean arterial pressure, and heart rate (p < 0.05). Kaempferol treatment prevented glomerular hypertrophy by reducing the increased glomerular cross-sectional area, glomerular tuft area, Bowman’s space area, glomerular volume, and the extent of renal tubulointerstitial fibrosis induced by hypertension (p < 0.05). Furthermore, animals in the L-NAME group showed elevated angiotensin-converting enzyme (ACE) activity and angiotensin II (Ang II) levels compared to those in the kaempferol-treated group (p < 0.05). Kaempferol treatment also reverted the elevations in levels of superoxide anions and malondialdehyde and reduced catalase and superoxide dismutase activity in hypertensive rats (p < 0.05). L-NAME-treated rats showed overexpression of angiotensin II receptor type 1 (AT1), nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), and matrix metalloproteinase-9 (MMP-9) proteins; conversely, the expression of these proteins was reduced in the kaempferol-treated group (p < 0.05). Conclusion. Kaempferol treatment alleviated renal remodelling induced in rats by chronic hypertension. These mechanisms may be associated with the inhibition of ACE activity and suppression of the Ang II/AT1 receptor/NOX4/MMP-9 cell signalling pathway in renal tissue.

Holothurians are prominent marine organisms in benthic ecosystems, exploited as food for centuries and, recently, as nutraceuticals. Moreover, they constitute a significant source of beneficial and medicinally valuable metabolites that have anticancer properties. Hypoxia, or low oxygen levels, and the stimulation of HIFs as a result of rapid cell proliferation and a restricted blood supply are characteristics shared by the majority of cancers, which give them resistance to standard treatment. The present study examines the effect of Holothuria tubulosa extract on the proliferation, HIF-α protein expression, and their transcriptional activity in hepatocarcinoma-derived Huh7 cells. Specimens of H. tubulosa were collected from the Aegean Sea, and their extract decreased the proliferation in Huh7 cells under normoxia and hypoxia in a dose-dependent manner by MTT assay. The extract modified HIF-1α protein expression by western blot analysis, downregulated hypoxia-induced VEGF promoter by luciferase assay, and decreased the expression of known HIF-1 and HIF-2-specific target genes, PGK and EPO, as revealed by real-time PCR. H. tubulosa extract had the ability to reduce the phosphorylated form of ERK1/2 explaining its inhibitory effect on proliferation and HIF activity. These data reveal new roles of H. tubulosa with promising anticancer properties in liver cancer cells.

Onopordopicrin (OPP), found in burdock leaves and stems, exerts antiallergic properties whose mechanism remains elusive. We aimed to elucidate its mechanism using rat basophilic leukemia cells in vitro. Purified OPP demonstrated concentration-dependent inhibition of degranulation after allergen or PMA/A23187 stimulation. OPP effectively suppressed TNF-α and PGD2 releases. However, OPP did not suppress the increase in intracellular Ca²⁺ concentration after allergen stimulation. The α, β-unsaturated carbonyl structure of OPP suggests potential electrophilic reactivity with polyfunctional thiol-trapping agents, such as cysteine residues. Indeed, the degranulation-inhibiting effect of OPP disappeared with the addition of cysteamine, which possesses a thiol group. I kappa B kinase β (IKKβ), which regulates degranulation in an NF-κB-independent manner, possesses a cysteine residue between the activation loop. Moreover, IKKβ plays an important role in TNF-α and PGD2 production. OPP was found to reduce IKKβ activity in a concentration-dependent manner. Together, our findings suggest that OPP exerts its antiallergic action via binding to cysteine residues in signal proteins such as IKKβ, thereby inhibiting their activation.

Despite being one of the most consumed analgesics worldwide, liver injury is an adverse effect of diclofenac (DF). In pursuit of reliable hepatoprotective natural remedies, this study aimed to investigate the potential protective effect of ferulic acid (FA) and its mechanism against DF-induced liver injury. Various network databases and datasets were used to collect targets corresponding to FA and DF-induced liver injury. Enrichment analyses of common targets were performed, a protein-protein interaction (PPI) network was constructed, the hub genes were identified, and the upstream miRNA interacting with the top hub gene was later predicted. A DF-induced liver injury rat model was established to verify FA’s protective effects, and the selected hub gene expression level with its upstream regulatory miRNA and a downstream set of targets was examined to elucidate the underlying mechanism. A total of 18 genes were identified as potential targets of FA to protect against DF-induced liver injury. Data from the enrichment and PPI analyses and the prediction of the upstream miRNAs indicated that the most worthwhile pair to study was miR-296-5p/Jun. In vivo findings showed that coadministration of FA significantly reduced the DF-induced alterations in the liver function indices, oxidative stress, and liver histology. Mechanistically, FA downregulated the expression of Jun, Bim, Bax, Casp3, IL-1β, IL-6, and TNF-α, whereas it upregulated the expression of rno-miR-296-5p and Bcl2. In conclusion, combining network pharmacology and an in vivo study revealed that miR-296-5p/Jun axis could mediate the mitigative effect of FA against DF-induced liver injury.

Hippocampal function can be impaired by diabetes mellitus (DM) and obesity. Abelmoschus esculentus (AE) fractions reportedly mitigate the symptoms of Alzheimer’s disease (AD) by downregulating dipeptidyl peptidase-4 (DPP-4)-mediated insulin resistance. AE extracted by alcohol (fraction 1, F1) and water (fraction 2, F2) contained quercetin glycosides and polysaccharides, respectively. In this study, we investigated whether AE affects hippocampal function in in vitro and in vivo systems. Our results indicate that F1 or F2 enhanced neurogenesis and synapse formation in palmitate-treated hippocampal neural cells, presumably by downregulating DPP-4. In db/db mice fed with high fat diet, the hippocampal insulin resistance correlated spatial recognition, with fraction F2 improving hippocampal function. Of note, the alteration of neurogenesis seems interconnecting with changes in gut microbiota. In summary, AE can improve hippocampal function, attenuate insulin resistance, and promote neurogenesis by regulating DPP-4. AE, particularly F2, has the potential to serve as an adjuvant in preventing DM-associated AD.

Curcuminoids are natural products with widespread biological activity mostly extracted from Curcuma longa and its family. In the current study, we report the first time to isolate curcuminoids from another phyto source. Three compounds (curcumin, desmethoxycurcumin (DMC), and bisdemethoxycurcumin (BDMC)) were isolated from the plant Deverra tortuosa using methanolic extract, which was then fractionated and separated by puriFlash. The purity of compounds was monitored by thin-layer chromatography and confirmed by high-performance liquid chromatography. The mass spectrometry identified the isolated compound by their electrospray ionisation. Molecular docking then demonstrated that curcumin and BDMC bind at the same cavity (187 Å) on SARS-CoV-2 M^pro protein indicating similarities while DMC binds to a cavity with a larger size (372 Å). Among the three curcuminoids, BDMC was shown to give the highest binding energy (−7.5 kcal/mol) followed by curcumin (−7.4 kcal/mol) and DMC (−7.3 kcal/mol). Calculating the half-maximal cytotoxic concentration and inhibitory median concentration of both DMC and BDMC showed low-to-moderate antiviral activity against SARS-CoV-2.