Journal of Food Biochemistry最新文献

Resveratrol (RES) is a nonflavonoid polyphenolic compound present in various plant species. Extensive research has confirmed the diverse biological activities of RES, rendering it highly promising for multiple industries. However, its stability is influenced by intrinsic factors, such as structure, and extrinsic factors, including light exposure, oxygen exposure, elevated temperature, and pH variations. RES also faces challenges related to low solubility, rapid metabolism, and limited bioavailability, which impede its application in the food and medical sectors. The objective of this study was to provide a comprehensive overview of the most up-to-date advancements in green and efficient RES production pathways and to evaluate RES instability and strategies for stabilization. The green and efficient production of RES is mainly achieved through plant extraction and biosynthesis. The RES plant extraction methods include deep eutectic solvent (DES) methods, ultrasound-assisted, supercritical fluid extraction (SFE), and enzyme-assisted extraction technology. The advantages and disadvantages of each method are compared in this paper. The biosynthesis of RES can produce a high yield in a short period, and the use of genetic engineering and other techniques to improve and optimize the yield has brought the possibility of the mass production of RES. More importantly, RES can be stabilized or protected by encapsulation, combined with other natural compounds, structurally modified and synthesized by chemo-enzymatic and other methods, which is of great significance for food, medicine, and clinical applications.

Atherosclerosis (AS), a chronic inflammatory vascular disease, is a major cause of cardiovascular morbidity and mortality worldwide. Indigo naturalis (IN) is a medicinal and edible plant with obvious pharmacological effects such as anti-inflammation, improving blood circulation, and antibacterial. However, its therapeutic efficacy and mechanism of action against AS remain unclear. This study aims to integrate network pharmacology, molecular docking, and in vitro and in vitro experimental evaluations to uncover the active components and multitarget mechanisms of IN against AS. 10 active ingredients and 96 related target genes were identified, and gene functional enrichment analysis suggested that the toll-like receptor signaling pathway plays a core role in IN’s action against AS. Molecular docking revealed strong binding affinities between IN’s key ingredients and hub genes. In vitro, IN regulated the expression of inflammatory factors, migration factors, and TLR4, NF-κB, and MyD88 proteins in cell inflammation models as predicted. In vivo, IN reduced aorta damage, cell apoptosis, blood lipids level, and inflammatory factors in LPS-induced AS mice, further downregulating the expression levels of TLR4, NF-κB, and MyD88. This study confirmed the feasibility of IN for AS treatment from an anti-inflammatory perspective, highlighting the TLR4/MyD88/NF-κB pathway as a critical mechanism. These findings provide a basis for developing IN as a potential candidate for anti-AS clinical application.

Ganodermalucidum (GL), commonly called Reishi mushroom, has been utilized in traditional medicine against multiple ailments including obesity and metabolic complications. The purpose of this study was to evaluate the ability of the powdered supplementation of GL (2.5% w/w of diet) and its ability to ameliorate obesity and associated metabolic alterations in high-carbohydrate-high-fat (HCHF) diet–fed obese female Wistar rats. Thus, after 56 days of feeding the mice with different treatments, we measured physiological parameters to evaluate the effect. Phytochemical analysis by HPLC identified the bioactive polyphenols in GL. Results demonstrated that GL supplementation significantly (p < 0.05) prevented the net rise in body weight and reduced organ weights and abdominal fat deposition in obese rats. It improved glucose intolerance, decreasing blood glucose level (6.2 nmol/L) compared to HCHF diet–induced obese rats (8.67 nmol/L). It also significantly ameliorated the plasma lipids parameters including total cholesterol (106.4 mg/dL), triglyceride, LDL-C (55.26 mg/dL), and VLDL-C, restored the elevated serum profiles of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), and elevated the antioxidant enzymes including superoxide dismutase (SOD) (42.58 U/g tissue), catalase (CAT) activities, and glutathione (GSH) (62.63 nmol/g tissue) in obese rats. Furthermore, GL prevented hepatic fat infiltration in HCHF diet–fed rats preventing steatosis. Different bioactive polyphenols including catechin, rutin, cinnamic acid, vanillic acid, quercetin, ferulic acid, and kaempferol were detected in GL by HPLC analysis, which might be responsible for its activity. Bangladeshi cultivated GL possesses antiobesity effect and is rich in phenolics that could prevent obesity-associated metabolic disorders.

This study investigates the potential antiobesity effects of Neptunea cumingii extract (NCE). Our findings illustrate that NCE effectively reduces lipid accumulation and triglyceride content, while simultaneously increasing free glycerol release. The reduction in lipid accumulation and induction of lipolysis were evidenced by the downregulation of lipogenesis proteins, such as fatty acid synthase and lipoprotein lipase, and the upregulation of hormone-sensitive lipase expression. Furthermore, the downregulation of adipogenic transcription factors, including peroxisome proliferator–activated receptor gamma, CCAAT/enhancer-binding protein α, and sterol regulatory element-binding protein 1, indicates the inhibition of adipocyte differentiation. Additionally, NCE treatment induced brown adipocyte phenotype by upregulating brown adipose tissue–specific proteins, such as uncoupling protein 1 and peroxisome proliferator–activated receptor-gamma coactivator 1α. Moreover, NCE led to the phosphorylation of AMPK, the master regulator of energy homeostasis. Pharmacological inhibition of AMPK using an AMPK inhibitor (Compound C) attenuated the lipogenesis inhibitory effect of NCE and reduced lipolysis and adipocyte browning. This suggests that AMPK activation is involved in these processes. GC–MS analysis reveals that NCE primarily consists of cholest-5-en-3-ol (27.15%) along with an array of fatty acids which possess favorable antiobesity properties. Collectively, these results highlight the potential of NCE as a lipid-lowering agent for the intervention of obesity.

Our preliminary investigation has unveiled that emodin may inhibit the neurotoxic effects of sodium fluoride (NaF) on SH-SY5Y cells by deactivating ERK and activating the Nrf2/HO-1 signaling pathway. This action thereby restores synaptic damage and reduces excessive reactive oxygen species (ROS) generation. To delve further into the neuroprotective effects of emodin on neuronal cells, our study revealed that 48 h of NaF treatment disrupted the balance between mitochondrial fission and fusion in SH-SY5Y cells. This disruption significantly upregulated proteins associated with pyroptosis pathways, including NLRP3, Caspase-1, IL-1β, and GSDMD expression, while inhibiting NF-κB phosphorylation. Notably, pretreatment with emodin effectively reinstated these alterations induced by NaF exposure, indicating its capacity to not only mitigate ROS production but also regulate mitochondrial dynamics and pyroptosis pathways. This counteraction of the toxic effects of NaF on SH-SY5Y cells provides valuable insights into the neuroprotective role of emodin.

Nonalcoholic fatty liver disease (NAFLD) has become a global pandemic, imposing a significant socioeconomic burden. Hepatic steatosis is a key pathological event in NAFLD. However, there is still lack of effective drugs for NAFLD treatment. Liquiritin (LIQ), derived from licorice root, exhibits antioxidative and anti-inflammatory properties, making it valuable in managing various conditions such as dermatological disorders, respiratory ailments, and gastritis. Here, we investigated the impact and underlying mechanisms of LIQ on hepatic steatosis in mouse primary hepatocytes (MPHs). Our study found that LIQ significantly decreased palmitic acid (PA)-induced lipid accumulation in MPHs. Additionally, LIQ remarkably increased the mRNA expression of Cpt1a, PPARα, Ehhadh, Cyp4a10, and Acox1, suggesting that LIQ achieves its lipid-lowering effect by regulating mitochondria-mediated lipid β-oxidation. Furthermore, the regulatory effect of LIQ on the mitochondrial oxidative phosphorylation (OXPHOS) process was confirmed by Seahorse analysis. Mechanistically, bioinformatics analysis predicted VEGFA as a crucial target mediating the beneficial effects of LIQ against PA-induced lipid accumulation in MPHs. Notably, treatment with purified VEGFA protein partially counteracted the lipid-lowering properties of LIQ. Additionally, our data showed that LIQ promoted VEGFA degradation through the ubiquitin–proteasome pathway. Therefore, our findings not only confirm the lipid-lowering effects of LIQ in MPHs but also identify VEGFA as its potential target. These results highlight the therapeutic promise of LIQ in managing NAFLD and introduce VEGFA as a novel target for treating hepatic steatosis.

Background: The role of docosahexaenoic acid (DHA) in fibrosis of other organs has been studied, but its function in oral submucous fibrosis (OSF) has not been reported. This study aimed to investigate the role and mechanism of DHA in OSF.

Methods: OSF rat and cell models were established induced by arecoline. Through a series of in vivo and in vitro experiments, the function of DHA in OSF was investigated. Mechanistically, the interaction of TGM-2 with HSP70A1A and p62 proteins was validated using co-immunoprecipitation. Additionally, in cells transfected with overexpression vectors of HSP70A1A or TGM-2 and treated with DHA and arecoline or co-treated with a p62 inhibitor XRK3F2 along with DHA and arecoline, the function of the DHA/HSP70A1A/TGM-2/p62 axis in OSF was explored.

Results: In vivo, arecoline caused severe pathological damage and fibrosis in rat oral mucosal tissues and induced overexpression of HSP70A1A. Arecoline treatment also elevated tissue ROS levels and the expression of α-SMA, Collagen I, TGM-2, and LC3 II/I, while decreasing tissue p62 protein expression and serum GSH levels. Treatment with DHA reversed these changes and improved the pathological damage and fibrosis in OSF rats. In vitro, arecoline induced the expression of HSP70A1A in a concentration-dependent manner, and DHA inhibited its expression by directly binding to HSP70A1A and reducing the expression of α-SMA, Collagen I, TGM-2, LC3 II/I, and ROS levels induced by arecoline in cells, while increasing p62 protein expression and GSH levels in cell supernatants. Furthermore, arecoline induced TGM-2 expression, and overexpression of HSP70A1A counteracted the protective effect of DHA on cells and the suppression of TGM-2 expression. TGM-2 interacted with HSP70A1A and p62 proteins. Overexpression of TGM-2 or treatment with XRK3F2 activated autophagy and abolished the protective effect of DHA on cells.

Conclusion: DHA inhibits p62-dependent autophagy through targeting the HSP70A1A/TGM-2 axis, thereby alleviating arecoline-induced OSF. These results suggest that DHA and its mediated autophagy regulation mechanism can be a therapeutic target for OSF.

Ultraviolet-C (UV-C), as a physical preservation technology, has the advantages of energy saving, safety, and sanitation and has broad application prospects in fruit storage. In this study, peach cultivated “Xiahui 5” was used as material to investigate the impact of UV-C on the softening, senescence, and postharvest quality of peaches. It was discovered that the application of UV-C postponed the peak of respiration, retarded the loss of firmness, and inhibited ethylene biosynthesis during peach fruit storage. The UV-C treatment led to the inhibition of the growth of soluble pectin content and the reduction of cellulose and hemicellulose content, together with the suppression of the activities of enzymes that break down cell walls. The application of UV-C treatment resulted in an increase in the total phenolic and flavonoid contents of peach fruit, accompanied by a corresponding enhancement in the activities of glutathione reductase (GR), catalase (CAT), ascorbate peroxidase (APX), and superoxide dismutase (SOD). This contributed to maintain the fruit’s normal redox balance and antioxidant capacity. The application of UV-C treatment resulted in a reduction in malondialdehyde (MDA) content and lipoxygenase (LOX) activity, thereby indicating that the oxidative damage of peach fruit during storage was inhibited by the UV-C. The application of UV-C maintained higher ATP content and induced the increase of cytochrome C oxidase (COX), succinate dehydrogenase (SDH), H⁺K⁺-ATPase, and Ca²⁺-ATPase activities involved in energy metabolism and had a significant impact in maintaining cell energy status. The findings suggest that UV-C treatment postpones peach fruit softening and senescence by maintaining cellular structure and energy homeostasis.

Background: Cow’s milk protein allergy (CMPA) is associated with activation of proinflammatory signaling pathways and overexpression of inflammatory mediators. Long noncoding RNA (LncRNA) HOX transcript antisense intergenic RNA (HOTAIR) is a LncRNA, which is involved in the occurrence and development of many biological processes and diseases. HOTAIR can prevent necrotizing enterocolitis. This study aims to explore the effect of milk protein on NCM-460 cells and its mechanism of action with HOTAIR.

Methods: NCM-460 cells were induced by cow’s milk protein to establish in vitro cell models. CCK-8 and EdU staining were used for evaluating the effects of cow’s milk protein on the viability and proliferation. ELISA was used for comparing the levels of inflammatory cytokines. TUNEL staining was conducted for evaluating the apoptosis. Expression levels of HOTAIR were detected by RT-qPCR. The expression of NF-κB signaling pathway–related molecules in cells was explored to evaluate the mechanism of HOTAIR in improving ALI.

Results: Cow’s milk protein decreased the viability NCM-460 cells and also decreased the expression of HOTAIR. Moreover, it can induce the antiproliferative and proapoptotic effects on NCM-460 cells, and overexpression of LncRNA HOTAIR can partially reverse the effects of cow’s milk protein. In addition, overexpression of LncRNA HOTAIR reversed the effects of cow’s milk protein on NF-κB signaling.

Conclusions: Cow’s milk protein may induce the allergy and inflammation in intestinal epithelial cells through regulating HOTAIR expression and NF-κB signaling pathways.

Introduction: Resveratrol and its analogs have potential therapeutic usage. Resveratrol is metabolized to various metabolites by gut microbiota, including dihydroresveratrol, lunularin, pinostilbene, and oxyresveratrol. However, they might have side effects by inhibiting human gonadal 3β-hydroxysteroid dehydrogenase 2 (h3β-HSD2) and rat homolog r3β-HSD1, thereby interfering with steroid biosynthesis.

Methods: Herein, we analyzed the inhibitory strength via in vitro assay, mode of action, structure–activity relationship, and docking simulation of resveratrol analogs on 3β-HSDs. Human KGN cell microsome was used as h3β-HSD2 source, and 90-day-old male Sprague–Dawley rat testicular microsome was used as r3β-HSD1 source. The conversion of pregnenolone to progesterone by 3β-HSDs was analyzed.

Results: IC₅₀ values for h3β-HSD2 were 4,4′-dihydroxystilbene (8.87 μM) > pinostilbene (10.51 μM) > resveratrol (50.04 μM) > lunularin (96.10 μM), while those for r3β-HSD1 were pinostilbene (5.11 μM) > 4,4′-dihydroxystilbene (15.16 μM) > resveratrol (26.58 μM) > lunularin (34.32 μM). Most resveratrol analogs were mixed/competitive inhibitors of both 3β-HSDs. Lipophilicity (LogP) and lowest binding energy determined the inhibitory strength. Docking analysis showed that resveratrol and its analogs bind to the NAD⁺-/steroid-binding sites of 3β-HSDs.

Conclusion: Resveratrol can inhibit both human and rat gonadal 3β-HSDs, thereby interfering with the metabolism and concentrations of steroid hormones such as progesterone, testosterone, and estradiol.

Practical Application: Consequently, this interference could hold significance for conditions related to hormone imbalances, such as polycystic ovary syndrome and certain cancers. Disorders marked by elevated levels of androgens, like hyperandrogenism, might find therapeutic benefit from interventions aimed at modulating 3β-HSD activity. Hence, resveratrol and its metabolites could present themselves as natural or supplementary treatment options for managing such conditions.