Probiotic-fermented tomato with hepatic lipid metabolism modulation effects: analysis of physicochemical properties, bioactivities, and potential bioactive compounds.

Lactiplantibacillus plantarum NCUH001046 (LP)-fermented tomatoes exhibited the potential to alleviate obesity in our previous study. This subsequent study further delves deeper into the effects of LP fermentation on the physicochemical properties, bioactivities, and hepatic lipid metabolism modulation of tomatoes, as well as the analysis of potential bioactive compounds exerting obesity-alleviating effects. Results showed that after LP fermentation, viable bacterial counts peaked at 9.11 log CFU mL-1 and sugar decreased, while organic acids, umami amino acids, total phenols, and total flavonoids increased. LP fermentation also improved the inhibition capacities of three digestive enzyme activities and Enterobacter cloacae growth, as well as antioxidant activities. Western blot results indicated that fermented tomatoes, especially live probiotic-fermented tomatoes (LFT), showed improved effects compared to unfermented tomatoes in reducing hepatic lipid accumulation by activating the AMPK signal pathway. UHPLC-Q-TOF/MS-based untargeted metabolomics analysis showed that chlorogenic acid, capsiate, tiliroside, irisflorentin, and homoeriodictyol levels increased after fermentation. Subsequent cell culture assays demonstrated that irisflorentin and homoeriodictyol reduced lipid accumulation via enhancing AMPK expression in oleic acid-induced hyperlipidemic HepG2 cells. Furthermore, Spearman's correlation analysis indicated that the five phenols were positively associated with hepatic AMPK pathway activation. Consequently, it could be inferred that the five phenols may be potential bioactive compounds in LFT to alleviate obesity and lipid metabolism disorders. In summary, these findings underscored the transformative potential of LP fermentation in enhancing the bioactive profile of tomatoes and augmenting its capacity to alleviate obesity and lipid metabolism disorders. This study furnished theoretical underpinnings for the functional investigation of probiotic-fermented plant-based foods.

Effects of fermentation with Lactiplantibacillus plantarum NCU116 on the antihypertensive activity and protein structure of black sesame seed.

Effects of fermentation by Lactobacillus Plantarum NCU116 on the antihypertensive potential of black sesame seed (BSS) and structure characteristics of fermented black sesame seed protein (FBSSP) were investigated. Angiotensin-I-converting enzyme (ACE) inhibition and zinc chelating ability of fermented black sesame seed hydrolysate (FBSSH) reached the highest of 60.78 ± 3.67 % and 2.93 ± 0.04 mg/mL at 48 h and 60 h of fermentation, respectively. Additionally, the antioxidant activities of FBSSH and surface hydrophobicity of FBSSP were increased noticeably by fermentation. The α-helix and ß-rotation of FBSSP tended to decrease and increase, respectively, during fermentation. Correlation analysis indicated strong positive relationships between ß-turn and ACE inhibition activity as well as zinc chelating ability with correlation coefficients r of 0.8976 and 0.8932. Importantly, novel ACE inhibitory peptides LLLPYY (IC50 = 12.20 µM) and ALIPSF (IC50 = 558.99 µM) were screened from FBSSH at 48 h using in silico method. Both peptides showed high antioxidant activities in vitro. Molecular docking analysis demonstrated that the hydrogen bond connected with zinc ions of ACE mainly attributed to the potent ACE inhibitory activity of LLLPYY. The findings indicated that fermentation by Lactobacillus Plantarum NCU116 is an effective method to enhance the antihypertensive potential of BSS.

Characterization, mechanism and in vivo validation of Helicobacter pylori antagonism by probiotics screened from infants' feces and oral cavity.

Helicobacter pylori (H. pylori) infection is a major cause of chronic gastritis, intestinal metaplasia, and gastric carcinoma. Antibiotics, the conventional regimen for eliminating H. pylori, cause severe bacterial resistance, gut dysbiosis and hepatic insufficiency. Here, fifty lactic acid bacteria (LAB) were initially screened out of 266 strains obtained from infants' feces and oral cavity. The antagonistic properties of these 50 strains against H. pylori were investigated. Based on eight metrics combined with principal component analysis, three LAB with probiotic function and excellent anti-H. pylori capacity were affirmed. Combining dynamics test, metabolite assays, adhesion assays, co-cultivation experiments, and SEM and TEM observations, LAB were found to antagonize H. pylori by causing coccoid conversion and intercellular adhesion. Furthermore, it was found that LAB antagonized H. pylori by four pathways, i.e., production of anti-H. pylori substances, inhibition of H. pylori colonization, enhancement of the gastric mucosal barrier, and anti-inflammatory effect. In addition, animal model experiments verified that the final screened superior strain L. salivarius NCUH062003 had anti-H. pylori activity in vivo. LAB also reduced IL-8 secretion, ultimately alleviating the inflammatory response of gastric mucosa. Whole genome sequencing (WGS) data showed that the NCUH062003 genome contained the secondary metabolite biosynthesis gene cluster T3PKS. Furthermore, NCUH062003 had a strong energy metabolism and substance transport capacity, and produced a small molecule heat stable peptide (SHSP, 4.1-6.5 kDa). Meanwhile, LAB proved to be safe through antibiotic susceptibility testing and CARD database comparisons.

Natural foods resources and dietary ingredients for the amelioration of Helicobacter pylori infection.

Helicobacter pylori (H. pylori) is a gastric-persistent pathogen that can cause peptic ulcer disease, gastric cancer, and mucosal-associated lymphoid tissue lymphoma. This pathogen is commonly treated with antibiotic-based triple or quadruple therapy. However, antibiotic therapy could result in the bacterial resistance, imbalance of gut microbiota, and damage to the liver and kidneys, etc. Therefore, there is an urgent need for alternative therapeutic strategies. Interestingly, natural food resources, like vegetables, fruits, spices, and edible herbs, have potent inhibitory effects on H. pylori. In this review, we systematically summarized these foods with supporting evidence from both animal and clinical studies. The results have indicated that natural foods may possess temporary inhibition effect on H. pylori rather than durable eradication, and may help to reduce H. pylori colonization, enhance the effect of antibiotics and modulate the host's immune response.

Modulation of the Microbiome-Fat-Liver Axis by Lactic Acid Bacteria: A Potential Alleviated Role in High-Fat-Diet-Induced Obese Mice.

The major characteristics of obesity are abnormal lipid metabolism, chronic inflammation, and imbalanced gut microbiota. It has been reported that lactic acid bacteria (LAB) possess potential for alleviating obesity, considering which the strain-specific functions and diverse mechanisms and the roles and mechanisms of various LAB are worthy of investigation. This study aimed to validate and investigate the alleviating effects and underlying mechanisms of three LAB strains, Lactiplantibacillus plantarum NCUH001046 (LP), Limosilactobacillus reuteri NCUH064003, and Limosilactobacillus fermentum NCUH003068 (LF), in high-fat-diet-induced obese mice. The findings demonstrated that the three strains, particularly LP, suppressed body weight gain and fat deposition; ameliorated lipid disorders, liver and adipocyte morphology, and chronic low-grade inflammation; and reduced lipid synthesis via activating the adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling pathway. In addition, LP and LF decreased the enrichment of bacteria positively correlated with obesity, like Mucispirillum, Olsenella, and Streptococcus, but facilitated the growth of beneficial bacteria negatively correlated with obesity, like Roseburia, Coprococcus, and Bacteroides, along with increasing the short-chain fatty acid levels. It is deduced that the underlying alleviating mechanism of LP was to modulate the hepatic AMPK signaling pathway and gut microbiota by the microbiome-fat-liver axis to alleviate obesity development. In conclusion, as a diet supplement, LP has promising potential in obesity prevention and treatment.

Advanced Glycation End Products and Nitrosamines in Sausages Influenced by Processing Parameters, Food Additives and Fat during Thermal Processing.

Advanced glycation end products (AGEs) and nitrosamines (NAs) in sausage are associated with pathogenic and carcinogenic risks. However, the multiple reaction parameters affecting the production of AGEs and NAs during sausage processing remain unclear. This experiment evaluated the effects of processing parameters, food additives and fat ratios on the formation of AGEs and NAs in sausages. The results showed a 2-3-fold increase in Nε-(carboxymethyl)lysine (CML) and Nε-(carboxyethyl)lysine (CEL) when the sausage processing temperature was increased from 90 °C to 130 °C, and N-nitrosodimethylamine (NDEA) increased from 3.68 ng/g to 6.41 ng/g. The addition of salt inhibited the formation of AGEs and NAs, and the inhibitory ability of 2 g/100 g of salt was 63.6% for CML and 36.5% for N-nitrosodimethylamine (NDMA). The addition of 10 mg/kg nitrite to sausages reduced CML formation by 43.9%, however, nitrite had a significant contribution to the formation of NAs. The addition of fat only slightly contributed to the production of CML. In addition, the relationship between α-dicarbonyl compounds and the formation of AGEs was investigated by measuring the changes in α-dicarbonyl compounds in sausages. The results showed two trends of AGEs and α-dicarbonyl compounds: AGEs increased with the increase in α-dicarbonyl compounds and AGE level increased but α-dicarbonyl compound level decreased.

Acetylated polysaccharides: Synthesis, physicochemical properties, bioactivities, and food applications.

Polysaccharides are biomacromolecular widely applied in the food industry, as gelling agents, thickeners and health supplements. As hydrophobic groups, acetyls provide amphiphilicity to polysaccharides with numerous hydroxyl groups, which greatly expand the presence of polysaccharides in organic organisms and various chemical environments. Acetylation could result in diverseness and promotion of the structure of polysaccharides, which improve the physicochemical properties and biological activities. High efficient and environmentally friendly access to acetylated derivatives of different polysaccharides is being explored. This review discusses and summarizes acetylated polysaccharides in terms of synthetic methods, physicochemical properties and biological activities and emphasizes the structure-effect relationships introduced by acetyl groups to reveal the potential mechanism of acetylated polysaccharides. Acetyls with different contents and substitution sites could change the molecular weight, monosaccharide composition and spatial architecture of polysaccharides, resulting in differences among properties such as water solubility, emulsification and crystallinity. Coupled with acetyls, polysaccharides have increased antioxidant, immunomodulatory, antitumor, and pro-prebiotic capacities. In addition, their possible applications have also been discussed in green food materials, bioactive ingredient carriers and functional food products, indicating that acetylated polysaccharides hold a clear vision in food health and industrial development.

Comprehensive characterization of glucomannans from different sources to trigger moderate macrophages immune activation.

Macrophage activation is involved in the outcome of many diseases and is recognized as one of the best targets for disease intervention. Glucomannans had shown promising immunomodulatory potential. Herein, the activation performance of macrophages by glucomannans from different sources was thoroughly investigated. Glucomannans triggered the immune activation of macrophages, which was mainly manifested in increasing the secretion of immune effector molecules, enhancing the endocytosis and phagocytosis of macrophages, and selectively facilitating the expression of M1 phenotype. The participation of NF-κB and MAPK signaling pathways further validated the immune activation of macrophages by glucomannans. Correlation analysis indicated acetyl might be a feasible target for glucomannans to induce immune activation and the molecular weight (Mw) of glucomannans was also inseparable from the performance of immune activation. In conclusion, glucomannans showed a moderate immune activation effect on macrophages, and their difference in immune activation was closely related to the acetyl content and Mw.

Aloe gel glucomannan induced colon cancer cell death via mitochondrial damage-driven PINK1/Parkin mitophagy pathway.

Mitophagy can selectively remove damaged mitochondria, which is critical in regulating mitochondrial homeostasis in diseases, such as cancer. Herein, we found that Aloe gel glucomannan (AGP) significantly inhibited the proliferation of colon cancer cells. RNA-seq analysis revealed that AGP upregulated autophagy, lysosome and mitochondrial fission signal pathways in colon cancer cell line CT26. Notably, AGP induced the accumulation of impaired and reactive oxygen species (ROS)-generating mitochondria, which triggered excessive mitophagy. Interestingly, the mitophagy activator enhanced AGP-induced mitophagy and cytotoxicity, whereas the mitophagy inhibitor reversed the influence of AGP. Furthermore, activation of PINK1/Parkin mitophagy pathway and transcription factor EB (TFEB) signaling was dependent on ROS overproduction. Taken together, these results indicated that AGP induced cytotoxic mitophagy through ROS-related PINK1/Parkin pathway and TFEB activation in CT26 cells. The research would provide theoretical basis for the development of AGP as a promising anticancer agent.

Gastroprotective activity of polysaccharide from the fruiting body of Hericium erinaceus against acetic acid-induced gastric ulcer in rats and structure of one bioactive fraction.

This study aimed at investigating gastroprotective activity of Hericium erinaceus polysaccharide (HEP) and characterizing one of its bioactive fractions. Acetic acid-induced gastric ulcer (GU) rat model was used to evaluate the gastroprotective activity of HEP, while H2O2-induced injury GES-1 cell model was conducted to screen the bioactive fractions from HEP. Moreover, one of the bioactive fractions was characterized using methylation and 1D/2D NMR analysis. Results indicated HEP treatment could ameliorate acetic acid-induced GU in rats. HEP supplement decreased levels of interleukin-6, tumor necrosis factor-α and malondialdehyde and myeloperoxidase activity, and increased releases of nitric oxide, prostaglandin E2, epidermal growth factor, vascular endothelial growth factor and basic fibroblast growth factor and superoxide dismutase activity in gastric tissues of ulcerated rats. Five purified polysaccharides from HEP were screened to be bioactive fractions with cytoprotection on H2O2-induced injury in GES-1 cells. Among them, RP-S was characterized to be a (1 â†’ 6)-ß-D-glucan, whose backbone was composed of →6)-ß-D-Glcp-(1 â†’ residue and branched with T-ß-D-Glcp-(1 â†’ residue at O-3 position. In conclusion, HEP possessed gastroprotection against acetic acid-induced GU in rats and one of its bioactive fractions was a ß-D-glucan. This study supports the utilization of HEP in anti-GU and provides evidences for the structure of gastroprotective HEP.

4-[1-Ethyl-1-methylhexy]-phenol induces apoptosis and interrupts Ca2+ homeostasis via ROS pathway in Sertoli TM4 cells.

Biological effect of an individual nonylphenol (NP) isomer extremely relies upon the side chain structure. This research was designed to evaluate the impact of NP isomer, 4-[1-ethyl-1-methylhexy]-phenol (NP65), on Sertoli cells in vitro. Sertoli TM4 cells were exposed to various concentration (0, 0.1, 1, 10, or 20 µM) of NP65 for 24 h, and the outcomes indicated that treatment of NP65 induced reactive oxygen species (ROS) generation, oxidative stress, and apoptosis for Sertoli TM4 cells. In addition, it was found that NP65 exposure affected homeostasis of Ca2+ in Sertoli TM4 cells by increasing cytoplasm [Ca2+]i, inhibiting Ca2+-ATPase activity and decreasing cyclic adenosine monophosphate (cAMP) concentration. Pretreatment with ROS scavenger, N-acetylcysteine (NAC), attenuated NP65-induced oxidative stress as well as apoptosis for TM4 cells. Furthermore, NAC blocked NP65-induced disorders of Ca2+ homeostasis by attenuating the growth of intracellular [Ca2+]i and the inhibition of Ca2+-ATPase and cAMP activities. Thus, we have demonstrated that NP65 induced apoptosis as well as acted as a potent inhibitor of Ca2+-ATPase activity and resulted in disorder of Ca2+ homeostasis in Sertoli TM4 cells; ROS participated in the process. Our results supported the view that oxidative stress acted an essential role within the development of apoptosis and Ca2+ overload in TM4 cells as a consequence of NP65 stimulation.

Natural Antioxidants and Hydrocolloids as a Mitigation Strategy to Inhibit Advanced Glycation End Products (AGEs) and 5-Hydroxymethylfurfural (HMF) in Butter Cookies.

Maillard reaction during food processing contributes to the formation of some unpleasant heat-induced toxicants including advanced glycation end products (AGEs) and 5-hydroxymethylfurfural (HMF). The current study prepared butter cookies fortified with two dietary natural antioxidants (catechins and curcumin) and two dietary hydrocolloids (pectin and chitosan), and investigated their effects on formation of free Nε-(carboxymethyl)lysine (CML)/Nε-(carboxyethyl)lysine (CEL), protein-bound CML/CEL and HMF and on the sensory qualities of butter cookies. Meanwhile, three typical α-dicarbonyl compounds were also determined to identify possible correlations between α-dicarbonyl intermediates and formation of these harmful heat-induced products in butter cookies. Experimental data showed that catechin exhibited the strongest inhibitory effects on formation of AGEs and HMF, but its addition would impair the color and taste of cookies. On the other hand, chitosan was not so effective in inhibiting AGEs and HMF as compared to catechin, but its addition could increase the sensory qualities of butter cookies.

Genistein interferes with antitumor effects of cisplatin in an ovariectomized breast cancer xenograft tumor model.

Genistein (GEN) has been demonstrated to interfere with antitumor effects of cisplatin (CIS) in vitro. To analyze whether these findings are also relevant in vivo, we examined the effects of combined GEN and CIS treatment in an ovariectomized nude mouse breast cancer xenograft model. Tumor growth and markers for antitumor activity were determined after three weeks of treatment. Furthermore, the concentrations of GEN metabolites were measured in serum, liver, and xenograft tumor tissues using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Three weeks' oral exposure to GEN at a dose of 5 mg kg-1·d-1 resulted in an average concentration of total GEN metabolite equivalent as high as 0.2729 nmol g-1 wet weight in xenograft tumor tissues. At this dosage, GEN significantly antagonized the antitumor effects of CIS. Mechanistically, GEN blocked both the inhibition of cell proliferation and induction of apoptosis triggered by CIS. Moreover, GEN concentrations in xenograft tumor tissues were found to be significantly higher than in serum and liver. In conclusion, our findings suggested that oral GEN exposure at a level comparable to dietary exposure in humans could interfere with CIS chemotherapy.

Dendrobium officinale polysaccharide triggers mitochondrial disorder to induce colon cancer cell death via ROS-AMPK-autophagy pathway.

The homeostasis between mitochondrial function and autophagy is crucial to the physiological activity of cancer cells, and its mechanism is conducive to the development of anti-tumor drugs. Here, we aimed to explore the effect and mechanism of Dendrobium officinale polysaccharide (DOP) on colon cancer cell line CT26. Our data showed that DOP significantly inhibited the proliferation of CT26 cells and elevated autophagy level. Moreover, DOP disrupted mitochondrial function through increasing reactive oxygen species (ROS) and reducing mitochondrial membrane potential (MMP), thereby impairing ATP biosynthesis, which activated AMPK/mTOR autophagy signaling. Intriguingly, the further experiments demonstrated that DOP-induced cytotoxicity, excessive autophagy and mitochondrial dysfunction were reversed after CT26 cells pretreated with antioxidant (N-acetyl-l-cysteine). Herein, these findings implied that DOP-induced mitochondrial dysfunction and cytotoxic autophagy repressed the propagation of CT26 cells via ROS-ATP-AMPK signaling, providing a new opinion for the study of antineoplastic drugs.

Composition of bound polyphenols from carrot dietary fiber and its in vivo and in vitro antioxidant activity.

Qualitative analysis of bound polyphenols from carrot dietary fiber (CDF-PP) was performed by ultra-performance liquid chromatography equipped with an electrospray ionization and quadrupole time-of-flight mass spectrometry (UPLC-ESI-QTOF-MS/MS). Eleven organic acids, nine hydroxybenzoic acids and derivatives, six hydroxycinnamic acids and derivatives, four phenolic alcohols and derivatives, three flavonoids and derivatives, seven esters and derivatives, two other compounds, were detected by matching their retention times, secondary mass spectrometry fragment information with authentic standards or literature data. Furthermore, in vitro antioxidant activity was determined by different kinds of assays, including DPPH, ORAC, PSC, demonstrated that CDF-PP could scavenge radicals in a dose dependent manner. Moreover, CDF-PP exhibited significantly reactive oxygen species (ROS) scavenging activity in living Caenorhabditis elegans. To our knowledge, this is the first comprehensive research to investigate composition and in vitro/in vivo antioxidant activity of bound polyphenols in CDF, which implied that CDF-PP could be a promising source of antioxidants.

Screening, Safety Evaluation, and Mechanism of Two Lactobacillus fermentum Strains in Reducing the Translocation of Staphylococcus aureus in the Caco-2 Monolayer Model.

Staphylococcus aureus is a common commensal of humans, and its translocation from gastrointestine to peripheral organs and tissues could cause severe diseases and complications. This study focuses on the screening and characterization of Lactobacillus strains with significant inhibitory effect on the translocation of S. aureus through Caco-2 monolayers. First, strains with strong affinity for mucin and Caco-2 cells were obtained, via microtiter plate assay and adhesion assay, respectively. Obtained bacteria were further tested for their inhibitory effects on the growth of S. aureus by well diffusion assay. Subsequently, two strains preincubated with Caco-2 monolayers were found to inhibit the translocation of S. aureus CMCC26003 by 80.95 and 43.96%, respectively, via the transcellular translocation assay. These two strains were then identified to be Lactobacillus fermentum NCU3087 and L. fermentum NCU3088. Second, the mechanism of inhibition was investigated by analyzing the relative concentration of tight junction proteins and proinflammatory cytokines of Caco-2 cells, by Western blot and enzyme-linked immunosorbent assay, respectively. Results showed that both NCU3087 and NCU3088 significantly attenuated the degradation of occludin, claudin-1, ZO-1, and JAM-1 and suppressed the secretion of interleukin 6 and tumor necrosis factor-α induced by S. aureus, to different extent. Moreover, two Lactobacillus strains could barely translocate the Caco-2 monolayers, had no hemolytic activity, displayed strong resistance to gastrointestinal fluids, and were sensitive or moderate sensitive to nine clinically relevant antibiotics. Collectively, this study identified two Lactobacillus strains with significant inhibitory effect on the translocation of S. aureus, and their safeness for application was evaluated, thereby providing potential solutions for prevention of S. aureus and prophylaxis of related diseases.

Polysaccharides from fermented Asparagus officinalis with Lactobacillus plantarum NCU116 alleviated liver injury via modulation of glutathione homeostasis, bile acid metabolism, and SCFA production.

Lactic acid bacteria strain (LAB) NCU116 fermented Asparagus officinalis polysaccharides (FAOP) have been proven to cause substantial changes in physicochemical properties such as monosaccharide composition and molecular weight, accounting for their enhanced immune activity than unprocessed Asparagus officinalis polysaccharides (AOP). In the current study, the hepatoprotective effects of FAOP in mice with cyclophosphamide (CTX)-induced hepatotoxicity were investigated. FAOP were more effective than AOP in alleviating CTX-induced hepatic damage, including inhibition of hepatic biochemical markers (ALT, AST, AKP and LDH) and pro-inflammatory cytokines (TNF-α and IL-1ß) as well as reinforcement of antioxidant systems (T-AOC, SOD, CAT, and MDA). In particular, compared with AOP, FAOP showed superior performance by promoting GSH biosynthesis, and normalizing the expression level of bile acid receptors (FXR and SHP) and key enzymes in bile acid synthesis (CYP7A1, CYP8B1 and CYP27A1). Modulation of disordered homeostasis of bile acids by FAOP can be attributed to the upregulation of hepatic short chain fatty acid (SCFA) receptors GPR41 and GPR109A as well as intestinal SCFA production. Furthermore, serum metabolomics study validated the hepatoprotective superiority of FAOP than AOP with evidence from variations in bile acid compositions and the construction of related metabolic pathways. Therefore, LAB NCU116 fermentation of Asparagus officinalis was practical and effective to obtain promising hepatoprotective polysaccharides, which might arise from enhanced SCFA production than unprocessed AOP.

Polysaccharide from the seeds of Plantago asiatica L. alleviates nonylphenol induced intestinal barrier injury by regulating tight junctions in human Caco-2 cell line.

The intestinal epithelium is known as an important barrier to protect the body from harmful pathogens or toxic substance that may induce intestinal barrier injury. The aim of this study was to investigate the effects of polysaccharide from the seeds of Plantago asiatica L. (PLP) on nonylphenol (NP) induced intestinal barrier injury in vitro. Caco-2 cells were pretreated with PLP, or co-cultured with PLP and NP simultaneously, and cytotoxicity, LDH leakage, transepithelial electrical resistance (TEER), FITC-dextran flux and tight junction (TJ) proteins were conducted to evaluate the intestinal barrier function. The results suggested that PLP pretreatment or co-culture with NP could significantly attenuated NP induced Caco-2 cytotoxicity, suppressed LDH release, restored the TEER value and paracellular permeability of Caco-2 monolayers, which were attributed to enhancing the TJ protein expressions. In addition, PLP co-cultured with NP possessed better protective effects against NP induced cytotoxicity. This study indicated that PLP assuaged NP induced intestinal barrier injury by increasing TJ, and threw light on the development of a dietary supplementation for preventing exogenous toxic substances induced intestinal barrier injury or improving intestinal TJ barrier function.

Cordyceps sinensis polysaccharide inhibits colon cancer cells growth by inducing apoptosis and autophagy flux blockage via mTOR signaling.

Cordyceps sinensis is thought to have anti-cancer effects, but its mechanisms remain elusive. In this study, we aimed to investigate the anti-cancer effect of Cordyceps sinensis polysaccharide (CSP) on human colon cancer cell line (HCT116) and its mechanism. Results indicated that CSP significantly inhibited the proliferation of HCT116 cells, increased autophagy and apoptosis, while blocked autophagy flux and lysosome formation. Further experiments showed that CSP decreased the expression of PI3K and phosphorylation level of AKT and mTOR, increased the expression of AMPKa and phosphorylation level of ULK1. In addition, repression of CSP-induced autophagy by bafilomycin (autophagy inhibitor) enhanced apoptosis and cell death of HCT116 cells. Hence, our findings suggested that CSP inhibited the proliferation of HCT116 cells by inducing apoptosis and autophagy flux blockage, which might be achieved through PI3K-AKT-mTOR and AMPK-mTOR-ULK1 signaling. CSP may be a potential therapeutic agent for colon cancer.

Regulatory effects of Ganoderma atrum polysaccharides on LPS-induced inflammatory macrophages model and intestinal-like Caco-2/macrophages co-culture inflammation model.

Lipopolysaccharide (LPS)-induced inflammatory macrophages model and intestinal-like Caco-2/macrophages co-culture inflammation model were established to evaluate the anti-inflammatory effect and underlying mechanism of Ganoderma atrum polysaccharides (PSG-1). It was found that PSG-1 reduced LPS-induced secretion of pro-inflammatory cytokine (TNF-α, IL-6 and IL-1ß), ROS levels, and inhibited the expression of COX-2 in LPS-stimulated inflammatory macrophages model and intestinal-like Caco-2/macrophages co-culture inflammation model. Furthermore, PSG-1 suppressed the LPS-induced activation of MAPKs signaling pathways, and regulated oxidative stress by activating the Nrf2/Keap1 signaling pathways. These above results indicated that PSG-1 not only has a direct anti-inflammatory effect in LPS-induced inflammatory macrophages model, but also has an indirect anti-inflammatory effect in intestinal-like Caco-2/macrophages co-culture inflammation model. These findings provide new insight of the mechanism underlying the anti-inflammatory activities of PSG-1, and facilitated the expansion of the application of PSG-1 in natural functional food.