Synergistic and Antagonistic Activity of Selected Dietary Phytochemicals against Oxidative Stress-Induced Injury in Cardiac H9c2 Cells via the Nrf2 Signaling Pathway.

The antioxidant activities of lycopene (LY), lutein (LU), chlorogenic acid (CA), and delphinidin (DP) were tested in vitro on H9c2 cell-based models. Some indicators, such as the generation of reactive oxygen (ROS), the quantification of cell antioxidant activity (CAA), and the expressions of SOD, GSH-Px, and CAT, were calculated to examine their antioxidant interactions. From our results, the phytochemical mixtures (M1: CA-LU: F3/10, M2: DP-CA: F7/10, M3: DP-LY: F5/10) displayed strong synergistic effects based on the generation of ROS and the quantification of CAA. However, great antagonistic bioactivities were seen in the combinations of LY-LU: F5/10 (M4), CA-LU: F9/10 (M5), and DP-LY: F7/10 (M6). Western blotting analysis indicated that the possible mechanism underlying the synergistic antioxidant interactions among phytochemical combinations was to enhance the accumulation of Nrf2 in the nucleus and the expression of its downstream antioxidant enzymes, HO-1 and GCLC. The combinations (M1-M3 groups) showed significant protection against the loss of mitochondrial membrane potential than individual groups to avoid excessive ROS production. The M4-M6 groups exerted antagonistic protective effects compared with the individual groups. In addition, lutein and lycopene absorption was improved more because of the presence of chlorogenic acid and delphinidin in the M1 and M3 groups, respectively. However, delphinidin significantly reduced the cellular uptake of lycopene in the M6 group. It appeared that antioxidant interactions of phytochemical combinations may contribute to the restoration of cellular redox homeostasis and lead to an improvement in diet quality and collocation.

Novel 3D printed TPMS scaffolds: microstructure, characteristics and applications in bone regeneration.

Bone defect disease seriously endangers human health and affects beauty and function. In the past five years, the three dimension (3D) printed radially graded triply periodic minimal surface (TPMS) porous scaffold has become a new solution for repairing bone defects. This review discusses 3D printing technologies and applications for TPMS scaffolds. To this end, the microstructural effects of 3D printed TPMS scaffolds on bone regeneration were reviewed and the structural characteristics of TPMS, which can promote bone regeneration, were introduced. Finally, the challenges and prospects of using TPMS scaffolds to treat bone defects were presented. This review is expected to stimulate the interest of bone tissue engineers in radially graded TPMS scaffolds and provide a reliable solution for the clinical treatment of personalised bone defects.

Genetic association of serum lipids and lipid-modifying targets with endometriosis: Trans-ethnic Mendelian-randomization and mediation analysis.

BACKGROUND: Prior observational research identified dyslipidemia as a risk factor for endometriosis (EMS) but the causal relationship remains unestablished due to inherent study limitations. METHODS: Genome-wide association study data for high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), and total cholesterol (TC) from European (EUR) and East Asian (EAS) ancestries were sourced from the Global Lipids Genetics Consortium. Multi-ancestry EMS data came from various datasets. Univariable Mendelian randomization (MR) examined causal links between serum lipids and EMS. Multivariable and mediation MR explored the influence of seven confounding factors and mediators. Drug-target MR investigates the association between lipid-lowering target genes identified in positive results and EMS. The primary method was inverse-variance weighted (IVW), with replication datasets and meta-analyses reinforcing causal associations. Sensitivity analyses included false discovery rate (FDR) correction, causal analysis using summary effect estimates (CAUSE), and colocalization analysis. RESULTS: IVW analysis in EUR ancestry showed a significant causal association between TG and increased EMS risk (OR = 1.112, 95% CI 1.033-1.198, P = 5.03×10-3, PFDR = 0.03), supported by replication and meta-analyses. CAUSE analysis confirmed unbiased results (P < 0.05). Multivariable and mediation MR revealed that systolic blood pressure (Mediation effect: 7.52%, P = 0.02) and total testosterone (Mediation effect: 10.79%, P = 0.01) partly mediated this relationship. No causal links were found between other lipid traits and EMS (P > 0.05 & PFDR > 0.05). In EAS ancestry, no causal relationships with EMS were detected (P > 0.05 & PFDR > 0.05). Drug-target MR indicated suggestive evidence for the influence of ANGPTL3 on EMS mediated through TG (OR = 0.798, 95% CI 0.670-0.951, P = 0.01, PFDR = 0.04, PP.H4 = 0.85%). CONCLUSIONS: This MR study in EUR ancestry indicated an increased EMS risk with higher serum TG levels.

SOX9 promotes stemness in the CAL27 cell line of tongue squamous cell carcinoma.

Tongue squamous cell carcinoma (TSCC) is a prevalent form of oral malignancy, with increasing incidence. Unfortunately, the 5-year survival rate for patients has not exceeded 50%. Studies have shown that sex-determining region Y box 9 (SOX9) correlates with malignancy and tumor stemness in a variety of tumors. To investigate the role of SOX9 in TSCC stemness, we analyzed its influence on various aspects of tumor biology, including cell proliferation, migration, invasion, sphere and clone formation, and drug resistance in TSCC. Our data suggest a close association between SOX9 expression and both the stemness phenotype and drug resistance in TSCC. Immunohistochemical experiments revealed a progressive increase of SOX9 expression in normal oral mucosa, paracancerous tissues, and tongue squamous carcinoma tissues. Furthermore, the expression of SOX9 was closely linked to the TNM stage, but not to lymph node metastasis or tumor diameter. SOX9 is a crucial gene in TSCC responsible for promoting the stemness function of cancer stem cells. Developing drugs that target SOX9 is extremely important in clinical settings.

New insights into dust emission mechanism in natural environments based on a series of field observations.

Most scholars have suggested that dust emission mainly depends on the bombardment of saltation particles based on wind tunnel experiments, because the cohesive forces between finer particles. However, in recent years, researchers have found that dust can be entrained directly in field. To detect the dust emission mechanism in natural environments, two types of field observations were carried out. Long-term observations were implemented on the shore of the Zu Lake, and the results show that the sediments contain large fractions of particulate matter <10 µm (PM10), which indicates that the entrainment of PM10 in sediment cannot solely depend on saltation bombardment. Short-term observations were conducted across the Desert Steppe, the Mu Us Sandy Land, and the shore of the Zu Lake, and a total of 31 plots were observed, which revealed that in most of the plots, the threshold of the friction velocities (TFVs) for PM10 entrainment was lower than for the entrainment of saltation particles, indicating that the PM10 was easier to entrain than the saltation particles. Large fractions of emitted PM10 were directly entrained, especially when the PM10 emission was continuous regardless of whether the PM10 contents of the soils were low or high, because the strong wind environment could renew the surface frequently and provided sufficient PM10 to be emitted. Based on our observations, we concluded that in natural environments, direct dust entrainment is the dominant dust emission mechanism, especially in continuous emission processes. Herein, we developed a parameterization scheme for continuous dust emission in natural environments, and this scheme can accurately simulate dust emission on different surfaces. The results of this study provide robust validation for the fact that direct dust entrainment dominates the dust emission mechanism in natural environments. In addition, the results provide valuable observation data for parameterization of dust emission.

Identification of OLA1 as a Novel Protein Target of Vitexin to Ameliorate Dextran Sulfate Sodium-Induced Colitis with Tissue Thermal Proteome Profiling.

Vitexin, which exists in various medicinal plants and food sources, has recently received increasing attention because of its anti-inflammatory properties. This study aims to identify the protein target of vitexin that ameliorates dextran sulfate sodium (DSS)-induced colitis. The results showed that vitexin not only alleviated the clinical symptoms and colonic damage in mice with DSS-induced colitis but also suppressed the colonic production of inflammatory cytokines (IL-1ß, IL-6, ICAM, and VCAM) and enhanced the expression of barrier-associated proteins (ZO-1, Occludin, and E-cadherin). Based on tissue thermal proteome profiling (Tissue-TPP) and molecular docking, OLA1 was creatively identified as a potential protein target for vitexin. Further siRNA-mediated knockdown of the OLA1 gene in Caco-2 cells demonstrated the ability of OLA1 to increase Nrf2 protein expression and, thus, mediated the anti-inflammatory effects of vitexin. Interaction of the OLA1-vitexin complex with Keap1 protein to disrupt the Keap1-Nrf2 interaction may be required for activating Nrf2. Our findings revealed a novel role for OLA1 as a protein target of vitexin that contributes to its anti-inflammatory action by activating Nrf2, which may provide a promising molecular mechanism for novel therapeutic strategies to treat colitis and the associated systemic inflammation.

Ly6D facilitates chemoresistance in laryngeal squamous cell carcinoma through miR-509/ß-catenin signaling pathway.

Chemotherapy resistance is a major limiting factor in the cure of patients with laryngeal squamous cell carcinoma (LSCC). Lymphocyte antigen 6 superfamily member D (Ly6D) is highly expressed in various tumors, but its role and underlying molecular mechanisms in chemoresistance of LSCC cells remains largely unclear. In this study, we reveal that overexpression of Ly6D facilitates LSCC cell chemoresistance, while Ly6D silencing abolishes this phenotype. Moreover, bioinformatics analysis, PCR array, and functional analysis confirmed that activation of the Wnt/ß-catenin pathway contributes to Ly6D-mediated chemoresistance. The genetic and pharmacological inhibition of ß-catenin compromises chemoresistance mediated by Ly6D overexpression. Mechanistically, Ly6D overexpression significantly attenuates the expression of miR-509-5p, thereby unleashing its target gene CTNNB1 to activate Wnt/ß-catenin pathway and ultimately promote chemoresistance. In contrast, Ly6D augmenting ß-catenin-mediated chemoresistance in LSCC cells were reversed by ectopic expression of miR-509-5p. Furthermore, ectopic expression of miR-509-5p markedly repressed the two other targets, MDM2 and FOXM1. Taken together, these data not only reveal the key role of Ly6D/miR-509-5p/ß-catenin in chemotherapy resistance, but also provide a new strategy for the clinical treatment of refractory LSCC.

Comprehensive quality evaluation of plant-based cheese analogues.

BACKGROUND: In recent years, there has been an increasing demand for plant-based cheese analogues, however, the protein content of plant-based cheeses currently on the market is generally low and cannot meet the nutritional needs of consumers. RESULTS: Based on the ideal value similarity method (TOPSIS) analysis the best recipe for plant-based cheese was 15% tapioca starch, 20% soy protein isolate, 7% gelatine as a quality enhancer and 15% coconut oil. The protein content of this plant-based cheese was170.1 g kg-1 , which was close to commercial dairy-based cheese and significantly higher than commercial plant-based cheese, The fat content was 114.7 g kg-1 , lower than that of commercial dairy-based cheese. The rheology properties show that the viscoelasticity of the plant-based cheese is higher than that of dairy-based cheese and commercial plant-based. The microstructure results show that the type and content of protein has a significant impact on its microstructure. The Fourier-transform infrared (FTIR) spectrum of the microstructure shows a characteristic value at 1700 cm-1 , because the starch was heated and leached to form a complex with lauric acid under the action of hydrogen bond. It can be inferred that in the interaction between plant-based cheese raw materials, fatty acids serve as a bridge between starch and protein. COUCLUSION: This study described the formula of plant-based cheese and the interaction mechanism between the ingredients, providing a basis for the development of subsequent plant-based cheese related products. © 2023 Society of Chemical Industry.

Pain management in patients with hepatocellular carcinoma after transcatheter arterial chemoembolisation: A retrospective study.

BACKGROUND: Pain after transcatheter arterial chemoembolisation (TACE) can seriously affect the prognosis of patients and the insertion of additional medical resources. AIM: To develop an early warning model for predicting pain after TACE to enable the implementation of preventive analgesic measures. METHODS: We retrospectively collected the clinical data of 857 patients (from January 2016 to January 2020) and prospectively enrolled 368 patients (from February 2020 to October 2022; as verification cohort) with hepatocellular carcinoma (HCC) who received TACE in the Hepatic Surgery Center of Tongji Hospital. Five predictive models were established using machine learning algorithms, namely, random forest model (RFM), support vector machine model, artificial neural network model, naive Bayes model and decision tree model. The efficacy of these models in predicting postoperative pain was evaluated through receiver operating characteristic curve analysis, decision curve analysis and clinical impact curve analysis. RESULTS: A total of 24 candidate variables were included in the predictive models using the iterative algorithms. Age, preoperative pain, number of embolised tumours, distance from the liver capsule, dosage of iodised oil and preoperative prothrombin activity were closely associated with postoperative pain. The accuracy of the predictive model was compared between the training [area under the curve (AUC) = 0.798; 95% confidence interval (CI): 0.745-0.851] and verification (AUC = 0.871; 95%CI: 0.818-0.924) cohorts, with RFM having the best predictive efficiency (training cohort: AUC = 0.869, 95%CI: 0.816-0.922; internal verification cohort: AUC = 0.871; 95%CI: 0.818-0.924). CONCLUSION: The five predictive models based on advanced machine learning algorithms, especially RFM, can accurately predict the risk of pain after TACE in patients with HCC. RFM can be used to assess the risk of pain for facilitating preventive treatment and improving the prognosis.

MYC-activated LINC00607 promotes hepatocellular carcinoma progression by regulating the miR-584-3p/ROCK1 axis.

BACKGROUND: There have been many reports of long non-coding RNAs (lncRNAs) in tumors, and abnormally expressed lncRNA is closely related to hepatocellular carcinoma (HCC). The mechanism of LINC00607 in HCC has not been reported. METHODS: We utilized qPCR to evaluate the RNA expression level. The mechanism of MYC binding to the LINC00607 promoter was revealed through chromatin immunoprecipitation assay and dual luciferase reporter assay. The proliferation and invasive ability were evaluated by CCK-8 and transwell assays. The relation between LINC00607 and miR-584-3p was assessed by RNA immunoprecipitation assay and dual luciferase reporter assay. The level of ROCK1 was evaluated by qPCR and western blot. RESULTS: In this research, we found that the expression of LINC00607 was higher in HCC tissues when compared with that in the adjacent non-tumor tissues. Meanwhile, MYC was observed to interact with the LINC00607 promoter, leading to the upregulation of LINC00607 in HCC. We further revealed that LINC00607 functioned as a sponge for miR-584-3p. Cell proliferation and migration assays showed that miR-584-3p may inhibit the HCC progression. Moreover, we found that the miR-584-3p inhibitor could reverse the effects of LINC00607 downregulation in HCC through rescue experiments. Through verification, miR-584-3p bound to the 3' UTR of ROCK1 to downregulate its expression. CONCLUSION: LINC00607 regulated by MYC can promote the proliferation, migration and invasion of HCC cells through the miR-584-3p/ROCK1 axis.

Polysaccharides from soybean residue fermented by Neurospora crassa alleviate DSS-induced gut barrier damage and microbiota disturbance in mice.

Soluble polysaccharides derived from microbial fermentation of agricultural by-products were considered as potential functional ingredients, primarily having probiotic properties. Herein, soluble polysaccharides (FSRP) were isolated from soybean residue fermented by Neurospora crassa, and FSRP mainly contained rhamnose, arabinose, fucose, mannose, glucose, and galactose, according to GC-MS analysis. To further investigate the protective effect of FSRP against colitis, dextran sulfate sodium induction (DSS)-treated mice were orally gavaged with FSRP (200 mg kg-1 d-1) or inulin (400 mg kg-1 d-1, a positive control) for 7 d. The results showed that DSS-treated mice displayed symptoms of body weight loss, atrophy, and histopathological changes of colon, as well as gut barrier damage, which were recovered after FSRP supplementation (similar to inulin). Furthermore, the beneficial effects of FSRP were linked to a decreased inflammatory response and increased protein expression of E-cadherin, claudin-1 and ZO-1. Illumina-MiSeq sequencing analysis revealed that FSRP increased microbial diversity and altered community structure. Specifically, FSRP could modulate the abundance of inflammation-related bacteria (such as Tenericutes, Clostridia, and Bacilli) to ameliorate colitis symptoms. Therefore, FSRP can relieve DSS-induced colitis, which is closely associated with reduced levels of inflammatory factors, improved gut barrier function and gut microbiota homeostasis.

Whole mulberry leaves as a promising functional food: From the alteration of phenolic compounds during spray drying and in vitro digestion.

This study investigated the potential of processing whole mulberry leaves as nutraceutical foods rich in phenolic compounds by spray drying with different drying aids. The results indicated that the spray-dried product 6 (24.2% whey protein isolate [WPI], 33.3% mulberry leaves solid, 38.7% maltodextrin, 3.8% soybean lecithin) with high WPI/mulberry leaves solid ratio possessed the best physical properties, the highest total phenolic compounds level and antioxidant capacity among all the products. Specifically, free chlorogenic acid and rutin were increased by two to three times, but free isoquercitrin and astragalin lost more than 50% in product 6 compared with fresh mulberry leaves. For in vitro digestion, rutin, isoquercitrin, and astragalin (the antioxidative phenolic compounds in mulberry leaves) showed higher bioaccessibility than chlorogenic acid (p < 0.05) in product 6. Meanwhile, the phenolic compounds bioaccessibility of product 6 was 10-20 times higher than that of fresh whole mulberry leaves. Considering the increased level and bioaccessibility of phenolic compounds, whole mulberry leaves could be developed as potential functional foods by spray drying under the protection of WPI. PRACTICAL APPLICATION: The spray-dried whole mulberry leaves can be consumed as a beverage, meal replacement powder, or used as additive during food processing.

A Comparison of Elevation, Perforation Rate, and Time Spent for the Crestal Sinus Elevation Intervened by Piezosurgery, CAS-Kit, and Osteotome in a Novel Goat Model.

Purpose: This study aimed to compare the differences among Piezosurgery, CAS-kit, and Osteotome regarding safe elevation, perforation rate, and time spent and to observe and analyze different sinus lifting efficacy of the three methods. Materials and Methods: Twenty-one fresh goat heads (42 sinuses) were investigated. CBCT images confirmed the feasibility of the goat model. The maxillary sinus was successively lifted to 5, 7, and 9 mm by Piezosurgery, CAS-kit, and Osteotome until the sinus membrane was perforated or lifted to 9 mm. In the end, final elevation, sinus perforation, and time spent were recorded. Results: Piezosurgery and CAS-kit lifted sinuses to relatively higher heights than did Osteotome (P = 0.000). Perforation rates (14.29, 21.43%) of the Piezosurgery and CAS-kit were far lower than that of the Osteotome (85.71%). In the Osteotome group, the time of lifting to 9 mm was significantly shorter than that of Piezosurgery and CAS-kit (P = 0.000). There was no statistical difference in time spent between the latter two (P = 0.115). Conclusions: The lifting height of the Osteotome was limited, but it took the shortest time for sinus lifting. Piezosurgery and CAS-kit had higher lifting heights and lower perforation rates compared with Osteotome.

IFP35 as a promising biomarker and therapeutic target for the syndromes induced by SARS-CoV-2 or influenza virus.

Previous studies have shown that the high mortality caused by viruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and influenza virus primarily results from complications of a cytokine storm. Therefore, it is critical to identify the key factors participating in the cytokine storm. Here we demonstrate that interferon-induced protein 35 (IFP35) plays an important role in the cytokine storm induced by SARS-CoV-2 and influenza virus infection. We find that the levels of serum IFP35 in individuals with SARS-CoV-2 correlates with severity of the syndrome. Using mouse model and cell assays, we show that IFP35 is released by lung epithelial cells and macrophages after SARS-CoV-2 or influenza virus infection. In addition, we show that administration of neutralizing antibodies against IFP35 considerably reduces lung injury and, thus, the mortality rate of mice exposed to viral infection. Our findings suggest that IFP35 serves as a biomarker and as a therapeutic target in virus-induced syndromes.

The identification of grain size genes by RapMap reveals directional selection during rice domestication.

Cloning quantitative trait locus (QTL) is time consuming and laborious, which hinders the understanding of natural variation and genetic diversity. Here, we introduce RapMap, a method for rapid multi-QTL mapping by employing F2 gradient populations (F2GPs) constructed by minor-phenotypic-difference accessions. The co-segregation standard of the single-locus genetic models ensures simultaneous integration of a three-in-one framework in RapMap i.e. detecting a real QTL, confirming its effect, and obtaining its near-isogenic line-like line (NIL-LL). We demonstrate the feasibility of RapMap by cloning eight rice grain-size genes using 15 F2GPs in three years. These genes explain a total of 75% of grain shape variation. Allele frequency analysis of these genes using a large germplasm collection reveals directional selection of the slender and long grains in indica rice domestication. In addition, major grain-size genes have been strongly selected during rice domestication. We think application of RapMap in crops will accelerate gene discovery and genomic breeding.

Long non-coding RNA CCDC183-AS1 acts AS a miR-589-5p sponge to promote the progression of hepatocellular carcinoma through regulating SKP1 expression.

BACKGROUND: Hepatocellular carcinoma (HCC) is a common type of malignant human cancer with high morbidity and poor prognosis, causing numerous deaths per year worldwide. Growing evidence has been demonstrated that long non-coding RNAs (lncRNAs) are closely associated with hepatocarcinogenesis and metastasis. However, the roles, functions, and working mechanisms of most lncRNAs in HCC remain poorly defined. METHODS: Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of CCDC183-AS1 in HCC tissues and cell lines. Cell proliferation, migration and invasion ability were evaluated by CCK-8 and transwell assay, respectively. Animal experiments were used to explore the role of CCDC183-AS1 and miR-589-5p in vivo. Bioinformatic analysis, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to confirm the regulatory relationship between CCDC183-AS1, miR-589-5p and SKP1. RESULTS: Significantly upregulated expression of CCDC183-AS1 was observed in both HCC tissues and cell lines. HCC patients with higher expression of CCDC183-AS1 had a poorer overall survival rate. Functionally, overexpression of CCDC183-AS1 markedly promoted HCC cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo, whereas the downregulation of CCDC183-AS1 exerted opposite effects. MiR-589-5p inhibitor counteracted the proliferation, migration and invasion inhibitory effects induced by CCDC183-AS1 silencing. Mechanistically, CCDC183-AS1 acted as a ceRNA through sponging miR-589-5p to offset its inhibitory effect on the target gene SKP1, then promoted the tumorigenesis of HCC. CONCLUSIONS: CCDC183-AS1 functions as an oncogene to promote HCC progression through the CCDC183-AS1/miR-589-5p/SKP1 axis. Our study provided a novel potential therapeutic target for HCC patients.

Long noncoding RNA SNHG14 promotes hepatocellular carcinoma progression by regulating miR-876-5p/SSR2 axis.

BACKGROUND: Aberrant expressions of long noncoding RNAs (lncRNAs) have been demonstrated to be related to the progress of HCC. The mechanisms that SNHG14 has participated in the development of HCC are obscure. METHODS: Quantitative real-time PCR (qRT-PCR) was used to measure the lncRNA, microRNA and mRNA expression level. Cell migration, invasion and proliferation ability were evaluated by transwell and CCK8 assays. The ceRNA regulatory mechanism of SNHG14 was evaluated by RNA immunoprecipitation (RIP) and dual luciferase reporter assay. Tumorigenesis mouse model was used to explore the roles of miR-876-5p in vivo. The protein levels of SSR2 were measured by western blot assay. RESULTS: In this study, we demonstrated that SNHG14 was highly expressed in HCC tissues, meanwhile, the elevated expression of SNHG14 predicted poor prognosis in patients with HCC. SNHG14 promoted proliferation and metastasis of HCC cells. We further revealed that SNHG14 functioned as a competing endogenous RNA (ceRNA) for miR-876-5p and that SSR2 was a downstream target of miR-876-5p in HCC. Transwell, CCK8 and animal experiments exhibited miR-876-5p inhibited HCC progression in vitro and in vivo. By conducting rescue experiments, we found the overexpression of SSR2 or knocking down the level of miR-876-5p could reverse the suppressive roles of SNHG14 depletion in HCC. CONCLUSION: SNHG14 promotes HCC progress by acting as a sponge of miR-876-5p to regulate the expression of SSR2 in HCC.

Synergistic antioxidant effects of phenolic acids and carotenes on H2O2-induced H9c2 cells: Role of cell membrane transporters.

Phenolic acids (caffeic acid, p-coumaric acid,) and carotenes (ß-carotene, lycopene) were mixed in different ratios to investigate antioxidant interactions on H2O2-induced H9c2 cells with ezetimibe (inhibitor of carotenes membrane transporters). Cellular uptake of carotenes, expression of membrane transporters, reactive oxygen species (ROS), nuclear factor erythroid 2-related factor 2 (Nrf2), NAD(P)H dehydrogenase quinone1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC) were analyzed. Results revealed that phenolic acids increased cellular uptake of carotenes and expression of their membrane transporters. Combination groups contained more phenolic acids showed synergistic effects. For example, ß-carotene: caffeic acid = 1:2 significantly suppressed the intracellular ROS (+EZT, 66.34 ±â€¯51.53%) and enhanced the accumulation of nucleus-Nrf2 (+EZT, 30.23 ±â€¯5.30) compared to the groups contained more ß-carotene (+EZT, ROS: 75.48 ±â€¯2.55%, nucleus-Nrf2: 19.48 ±â€¯4.22). This study provided an implication of functional foods formulation and demonstrated that antioxidant synergism may due to the up-regulation of carotenes membrane transporters by phenolic acids.

A polysaccharide from Fagopyrum esculentum Moench bee pollen alleviates microbiota dysbiosis to improve intestinal barrier function in antibiotic-treated mice.

Antibiotics are the most commonly used clinical drugs for anti-infection, but they can also destroy normal microorganisms and cause intestinal barrier dysfunction. To elucidate the effects and mechanism of a water-soluble polysaccharide from Fagopyrum esculentum Moench bee pollen (WFPP) on intestinal barrier integrity in antibiotic-treated mice, BALB/c mice were exposed to a broad-spectrum antibiotic (ceftriaxone) or not (control), and were administered low-, medium- and high-dose WFFP (100 mg kg-1, 200 mg kg-1 and 400 mg kg-1, respectively) daily by oral gavage for 3 weeks. Mice treated with ceftriaxone displayed symptoms of growth retardation, atrophy of immune organs including thymus and spleen, increased gut permeability, and intestinal barrier damage, which were restored after intervention with WFFP at different doses. Moreover, the beneficial effects of WFFP were closely associated with enhanced intestinal sIgA secretion and reduced inflammatory response. Furthermore 16S rDNA gene sequencing revealed that WFPP elevated microbial diversity and richness and changed the community structure, therefore, alleviating microbiota dysbiosis caused by ceftriaxone. Interestingly, WFPP could modulate the abundance of sIgA secretion-related bacteria (e.g. Proteobacteria) and inflammation-related bacteria (e.g. Enterococcus). Therefore, WFPP can relieve antibiotic-induced microbiota dysbiosis to improve intestinal barrier integrity by increasing intestinal sIgA secretion and inhibiting inflammation.