Fucoidan from Apostichopus japonicus ameliorates alcoholic liver disease by regulating gut-liver axis homeostasis.

Long-term and excessive alcohol consumption can lead to the development of alcoholic liver disease (ALD), characterized by oxidative damage, intestinal barrier injury, and disruption of intestinal microbiota. In this study, we extracted fucoidan (Aj-FUC) from Apostichopus japonicus using enzymatic methods and characterized its structure. The ALD model was established in male Balb/c mice using 56° Baijiu, with silymarin as a positive control. Mice were orally administered 100 mg/kg·bw and 300 mg/kg·bw of Aj-FUC for 28 days to evaluate its effects on liver injury in ALD mice and explore its potential role in modulating the gut-liver axis. The results showed significant improvements in histopathological changes and liver disease in the Aj-FUC group. Aj-FUC treatment significantly increased the levels of glutathione (GSH) and glutathione peroxidase (GSH-Px) while weakly reduced the elevation of malondialdehyde (MDA) induced by ALD. It also regulated the Nrf2/HO-1 signaling pathway, collectively alleviating hepatic oxidative stress. Aj-FUC intervention upregulated the expression of ZO-1 and Occludin, thus contributing to repair the intestinal barrier. Additionally, Aj-FUC increased the content of short-chain fatty acids (SCFAs) and regulated the imbalance in gut microbiota. These results suggested that Aj-FUC alleviates ALD by modulating the gut-liver axis homeostasis. It may prove to be a useful dietary supplement in the treatment of alcoholic liver damage.

Astaxanthin Ameliorates Skeletal Muscle Atrophy in Mice With Cancer Cachexia.

Astaxanthin (AST) is a natural marine carotenoid with a variety of biological activities. This study aimed to demonstrate the possible mechanisms by which AST improves skeletal muscle atrophy in cancer cachexia. In this study, the effects of different doses of AST (30 mg/kg b.w., 60 mg/kg b.w. and 120 mg/kg b.w.) on skeletal muscle functions were explored in mice with cancer cachexia. The results showed that AST (30, 60 and 120 mg/kg b.w.) could effectively protect cachexia mice from body weight and skeletal muscle loss. AST dose-dependently ameliorated the decrease in myofibres cross-sectional area and increased the expression of myosin heavy chain (MHC). AST treatment decreased both the serum and muscle level of IL-6 but not TNF-α in C26 tumor-bearing cachexia mice. Moreover, AST alleviated skeletal muscle atrophy by decreasing the expression of two muscle-specific E3 ligases MAFBx and MuRF-1. AST improved mitochondrial function by downregulating the levels of muscle Fis1, LC3B and Bax, upregulating the levels of muscle Mfn2 and Bcl-2. In conclusion, our study show that AST might be expected to be a nutritional supplement for cancer cachexia patients.

Astaxanthin exerts an adjunctive anti-cancer effect through the modulation of gut microbiota and mucosal immunity.

This study aimed to investigate the function of gut microbiota in astaxanthin's adjuvant anticancer effects. Our prior research demonstrated that astaxanthin enhanced the antitumor effects of sorafenib by enhancing the body's antitumor immune response; astaxanthin also regulated the intestinal flora composition of tumor-bearing mice. However, it is presently unknown whether this beneficial effect is dependent on the gut microbiota. We first used broad-spectrum antibiotics to eradicate gut microbiota of tumor-bearing mice, followed by the transplantation of fecal microbiota. The results of this study indicate that the beneficial effects of astaxanthin when combined with molecular targeting are dependent on the presence of intestinal microbiota. Astaxanthin facilitates the infiltration of CD8+ T lymphocytes into the tumor microenvironment and increases Granzyme B production by modulating the intestinal flora. Therefore, it strengthens the body's anti-tumor immune response and synergistically boosts the therapeutic efficacy of drugs. Astaxanthin stimulates the production of cuprocytes and mucus in the intestines by promoting the proliferation of Akkermansia. In addition, astaxanthin enhances the intestinal mucosal immunological function. Our research supports the unique ability of astaxanthin to sustain intestinal flora homeostasis and its function as a dietary immune booster for individuals with tumors.

Astaxanthin Augmented the Anti-Hepatocellular Carcinoma Efficacy of Sorafenib Through the Inhibition of the JAK2/STAT3 Signaling Pathway and Mitigation of Hypoxia within the Tumor Microenvironment.

SCOPE: The optimization of anti-cancer drug effectiveness through dietary modifications has garnered significant attention among researchers in recent times. Astaxanthin (AST) has been identified as a safe and biologically active dietary supplement. METHODS AND RESULTS: The tumor-bearing mice are treated with sorafenib, along with supplementation of 60 mg kg-1 AST during the treatment. The coadministration of AST and a subclinical dosage of 10 mg kg-1 sorafenib demonstrates a tumor inhibition rate of 76.5%, which is notably superior to the 45% inhibition rate observed with the clinical dosage of 30 mg kg-1 sorafenib (p < 0.05). The administration of AST leads to a tumor inhibition increase of around 25% when combined with the clinical dose of 30 mg kg-1 sorafenib (p <0.05). AST enhances the inhibitory effect of sorafenib on tumor angiogenesis through the JAK2/STAT3 signaling pathway. Furthermore, AST exhibits a reduction in hypoxia within the tumor microenvironment. CONCLUSION: The results suggest that AST supplement enhances the inhibitory effects of sorafenib on hepatocellular carcinoma. This study presents a new dietary management program for oncology patients.

Zein/hyaluronic acid nanoparticle stabilized Pickering emulsion for astaxanthin encapsulation.

Pickering emulsions have attracted considerable attention owing to the stability and functionality. In this study, zein/hyaluronic acid (ZH) nanoparticles were prepared and applied for stabilizing astaxanthin encapsulated Pickering emulsions. By non-covalent interaction between Zein and hyaluronic acid (HA), the conformation of zein changed and therefore improved the wettability of ZH nanoparticles. Unlike the spherical zein nanoparticles, ZH nanoparticles possessed a cross-linked structure with rough surface. Confocal laser scanning microscopy indicated that the nanoparticles accumulated at the oil-water interface. The Pickering emulsion stabilized by ZH nanoparticles exhibited high viscoelasticity and a solid-like behavior, as well as excellent stability during the storage. In vitro digestion results revealed that the presence of HA coating prevented the emulsion from pepsin hydrolysis and achieved efficient delivery of astaxanthin. This work confirmed that Pickering emulsion stabilized by ZH nanoparticles could be used as an effective deliver system for bioactive substances.

Astaxanthin slows down skeletal muscle atrophy in H22 tumor-bearing mice during sorafenib treatment by modulating the gut microbiota.

Astaxanthin is a carotenoid that is taken orally and has antitumor and anti-inflammatory properties. Our previous research demonstrated that astaxanthin alleviated skeletal muscle atrophy during sorafenib treatment in H22 tumor-bearing mice and altered the intestinal flora composition. However, the relationship between astaxanthin's amelioration of skeletal muscle atrophy in tumor-bearing mice and its ability to regulate intestinal flora is not clear. We used broad-spectrum antibiotics to create pseudo-sterile tumor-bearing mice, which we then used in fecal bacteria transplantation experiments. Our results indicate that the role of astaxanthin in ameliorating skeletal muscle atrophy during molecularly targeted therapy in mice with tumors is dependent on the intestinal flora. Astaxanthin substantially promoted the proliferation of Blautia, Parabacteroides, and Roseburia, altered the levels of metabolites in mouse serum, and primarily affected the amino acid metabolism of mice. Astaxanthin ameliorated skeletal muscle atrophy by promoting the activation of AKT/FOXO3a, which inhibited the expression of ubiquitination-degrading Fbx32 and MuRF1 and promoted myogenesis in skeletal muscle. Our study confirms that the intestinal flora is an important target for astaxanthin to combat skeletal muscle atrophy. Our research supports the use of astaxanthin as a nutritional supplement and intestinal microecological regulator for cancer patients.

Dietary supplementation with astaxanthin enhances anti-tumor immune response and aids the enhancement of molecularly targeted therapy for hepatocellular carcinoma.

Astaxanthin is a naturally occurring compound that possesses immunomodulatory properties. The results of our previous investigation indicated that astaxanthin has the potential to augment the anticancer effectiveness of the targeted medication sorafenib. However, the precise molecular mechanism underlying this phenomenon remains unclear. H22 tumor-bearing mice were treated with sorafenib at 30 mg kg-1 per day and their diet was supplemented with 60 mg kg-1 day-1 astaxanthin orally for a period of 18 days. The study revealed that the addition of astaxanthin to the diet facilitated the transition of tumor-associated macrophages from the M2 phenotype to the M1 phenotype. The application of astaxanthin resulted in an augmentation of CD8+ T cell infiltration within the tumor microenvironment through the activation of the CXCL9/CXCR3 signaling axis. Astaxanthin was found to enhance the production of cytokines that possess antitumor properties, including Granzyme B. Furthermore, the administration of astaxanthin resulted in alterations to the intestinal microbiota in H22-bearing mice, leading to the growth of bacteria that possess anti-tumor immune properties, such as Akkermansia. The findings of these studies indicate that astaxanthin has the potential to augment the immune response against tumors when used in conjunction with sorafenib. These studies offer a novel framework for the advancement of astaxanthin as an immunomodulatory agent and a dietary supplement for individuals with tumors.

Astaxanthin Supplementation Assists Sorafenib in Slowing Skeletal Muscle Atrophy in H22 Tumor-Bearing Mice via Reversing Abnormal Glucose Metabolism.

SCOPE: Cachexia, which is often marked by skeletal muscular atrophy, is one of the leading causes of death in cancer patients. Astaxanthin, a carotenoid obtained from marine organisms that can aid in the prevention and treatment of a variety of disorders. In this study, to assess whether astaxanthin ameliorates weight loss and skeletal muscle atrophy in sorafenib-treated hepatocellular carcinoma mice is aimed. METHODS AND RESULTS: H22 mice are treated with 30 mg kg-1  day-1 of sorafenib and 60 mg kg-1  day-1 of astaxanthin by gavage lasted for 18 days. Sorafenib does not delay skeletal muscle atrophy and weight loss, although it does not reduce tumor burden. Astaxanthin dramatically delays weight loss and skeletal muscle atrophy in sorafenib-treating mice, without affecting the food intake. Astaxanthin inhibits the tumor glycolysis, slows down gluconeogenesis, and improves insulin resistance in tumor-bearing mice. Astaxanthin increases glucose competition in skeletal muscle by targeting the PI3K/Akt/GLUT4 signaling pathway, and enhances glucose utilization efficiency in skeletal muscle, thereby slowing skeletal muscle atrophy. CONCLUSION: The findings show the significant potential of astaxanthin as nutritional supplements for cancer patients, as well as the notion that nutritional interventions should be implemented at the initiation of cancer treatment, as instead of waiting until cachexia sets in.

Identification and molecular docking study of sugarcane leaf-derived compounds as potent dipeptidyl peptidase IV, α-glucosidase, and α-amylase inhibitors.

BACKGROUND: Dipeptidyl peptidase-IV (DPP-IV), α-glucosidase, and α-amylase play a prominent role in regulating postprandial blood sugar levels, which are regarded as key targets for the treatment of type 2 diabetes mellitus (T2DM). The present study aimed to characterize bioactive compounds as potent crucial sugar metabolism enzyme inhibitors from sugarcane leaves by virtual screening. In total, 41 sugarcane leaf-derived compounds were used for the screening of multiple targets. Subsequently, the molecular mechanism and activity validation in vitro of the interaction between enzymes and compound were carried out. RESULTS: Flavonoid compound schaftoside was identified by molecular simulation and showed significant DPP-IV (0.1050 ± 1.22 mmol L-1 ), α-glucosidase (0.078 ± 0.06 mmol L-1 ), and α-amylase (0.3067 ± 0.35 mmol L-1 ) inhibitory effects. The residues ARG125 and TYR662 of DPP-IV may play crucial roles in inhibiting the activity of DPP-IV. Multiple hydrogen bonds and electrostatic interactions were exhibited between schaftoside and α-glucosidase. Molecular modeling revealed that schaftoside displays strong binding with the catalytic triad (ASP197, ASP300, and GLU233) of α-amylase. CONCLUSION: Our findings demonstrate that schaftoside from sugarcane leaves might be an edible for T2DM treatment." © 2023 Society of Chemical Industry.

Ameliorative Effect of Mannuronate Oligosaccharides on Hyperuricemic Mice via Promoting Uric Acid Excretion and Modulating Gut Microbiota.

Mannuronate oligosaccharide (MOS) is α-D-mannuronic acid polymer with 1,4-glycosidic linkages that possesses beneficial biological properties. The aim of this study was to investigate the hypouricemic effect of MOS in hyperuricemic mice and demonstrate the possible protective mechanisms involved. In this research, 200 mg/kg/day of MOS was orally administered to hyperuricemic mice for four weeks. The results showed that the MOS treatment significantly reduced the serum uric acid (SUA) level from 176.4 ± 7.9 µmol/L to 135.7 ± 10.9 µmol/L (p < 0.05). MOS alleviated the inflammatory response in the kidney. Moreover, MOS promoted uric acid excretion by regulating the protein levels of renal GLUT9, URAT1 and intestinal GLUT9, ABCG2. MOS modulated the gut microbiota in hyperuricemic mice and decreased the levels of Tyzzerella. In addition, research using antibiotic-induced pseudo-sterile mice demonstrated that the gut microbiota played a crucial role in reducing elevated serum uric acid of MOS in mice. In conclusion, MOS may be a potential candidate for alleviating HUA symptoms and regulating gut microbiota.

Alginate Oligosaccharides Prevent Dextran-Sulfate-Sodium-Induced Ulcerative Colitis via Enhancing Intestinal Barrier Function and Modulating Gut Microbiota.

Alginate oligosaccharides are degradation products of alginate and have attracted increasing attention due to their versatile biological functions. In the present study, C57BL/6 mice were used to assess the ameliorative effects and mechanisms of guluronate oligosaccharides (GAOS), mannuronic oligosaccharides (MAOS), and heterozygous alginate oligosaccharides (HAOS), which are the three alginate oligosaccharides of dextran sulfate sodium (DSS)-induced ulcerative colitis. The study showed that alginate oligosaccharides alleviated pathological histological damage by slowing down weight loss, inhibiting colonic length shortening, and reducing disease activity index (DAI) and histopathological scores. Alginate oligosaccharides modulated the colonic inflammatory response by reducing colonic MPO levels and downregulating the expression of IL-6 and IL-1ß. Alginate oligosaccharides reduced intestinal permeability and reversed intestinal barrier damage by increasing the number of goblet cells, decreasing LPS levels, downregulating Bax protein levels, upregulating Bcl-2 protein levels, and enhancing the expression of the E-cadherin. Furthermore, alginate oligosaccharides modulated the composition of the gut microbiota and restored the production of short-chain fatty acids (SCFAs), especially acetate and butyrate. In conclusion, our study provides a scientific basis for the role of alginate oligosaccharides in relieving ulcerative colitis.

Fabrication and characterization of core-shell gliadin/tremella polysaccharide nanoparticles for curcumin delivery: Encapsulation efficiency, physicochemical stability and bioaccessibility.

The objectives of the present study were to synthesize gliadin/tremella polysaccharide nanoparticles (Gli/TP NPs) as well as curcumin-loaded gliadin/tremella polysaccharide nanoparticles (Cur-Gli/TP NPs) and evaluate the encapsulation efficiency (EE), physicochemical stability and bioaccessibility of Cur-Gli/TP NPs. The physicochemical properties of the nanoparticles depended on the mass ratio of Gli to TP and pH values. The characterization of the Gli/TP NPs indicated that the prepared nanoparticles were the most stable when the Gli/TP mass ratio was 1:1 and pH was at 4.0-7.0. Afterward, prepared Cur-Gli/TP NPs at different pH values were studied. Compared with the EE of Cur (58.2%) in Cur-Gli NPs at pH 5.0, the EE of Cur (90.6%) in Cur-Gli/TP NPs at pH 5.0 was increased by 32.4%. Besides, the Cur-Gli/TP NPs possessed excellent physical stability, photostability, thermal stability and re-dispersibility than Cur-Gli NPs. Furthermore, the bioaccessibility of Cur reached 83.5% after encapsulation of Cur into Gli/TP NPs after in vitro digestion, indicating that Cur-Gli/TP NPs could improve curcumin bioaccessibility significantly. In summary, this study demonstrates that the new food-grade Gli/TP NPs possess high encapsulation efficiency, excellent stability and prominent nutraceutical bioaccessibility. Meanwhile, it contributes to expanding the application of TP in food-grade delivery systems.

The compound enzymatic hydrolysate of Neoporphyra haitanensis improved hyperglycemia and regulated the gut microbiome in high-fat diet-fed mice.

We previously found that the combination of protease and a novel ß-porphyranase Por16A_Wf may contribute to the deep-processing of laver. The purpose of the present study is to assess the hypoglycemic effect of the compound enzymatic hydrolysate (CEH) of Neoporphyra haitanensis. Thus, biochemical indexes related to diet-induced hyperglycemia were mainly detected using hematoxylin and eosin (H&E) staining, fluorescence quantitative PCR, and ultrahigh performance liquid chromatography-mass spectrometry (UPLC-MS). Then 16s rRNA gene sequencing was performed to analyze the effects of CEH on the gut microbiome in high-fat diet (HFD)-fed mice. The results suggested that CEH reduced the blood glucose level and alleviated insulin resistance. Possibly because CEH repressed intestinal α-glucosidase activity, inhibiting key enzymes (G6Pase and PEPCK) related to hepatic gluconeogenesis, and increased the expression of the enzyme (GLUT4) involved in peripheral glucose uptake. As potential indicators of hyperglycemia, total bile acids in the feces were reversed to the control levels after CEH intervention. Particularly, CEH decreased the content of tauro-α-muricholic acid (TαMCA) and ω-muricholic acid (ωMCA). Furthermore, CEH promoted the proliferation of beneficial bacteria (e.g. Parabacteroides), which may play a role in glycemic control. CEH also regulated the KEGG pathways associated with glycometabolism, such as "fructose and mannose metabolism". In summary, CEH supplementation has favorable effects on improving glucose metabolism and regulating the gut microbiome in HFD-fed mice. CEH has potential to be applied in the development of functional foods.

Colon and gut microbiota greatly affect the absorption and utilization of astaxanthin derived from Haematococcus pluvialis.

Astaxanthin has been widely favored as a health food supplement by individuals but its absorption in the body seems not to be satisfactory. In addition, the peak time of astaxanthin derived from Haematococcus pluvialis in the plasma was much longer than other carotenoids found in our previous research. Thus, it is necessary to explore the process that affects the absorption of astaxanthin in order to potentially find a novel approach to improve the absorption in the future. In this study, we confirmed that the colon has an ability to absorb astaxanthin and conducted acute feeding experiments with the treatment of antibiotics in C57BL/6J mice and chronic feeding experiments in germ-free (GF) mice to detect the relationship between the gut microbiota and the absorption of astaxanthin. Our study showed that the decrease of gut microbiota led to a less oral absorbability, which might be related to the decreased expression of SR-BI in the small intestine and the reduction of free form and Z-astaxanthin converted by the gut microbiota found in the vitro culture. The experiments of anaerobic culture also implied that Lactobacillus might play an important role in the absorption of astaxanthin.

Kappaphycus Alvarezii Compound Powder Prevents Chemotherapy-Induced Intestinal Mucositis in BALB/c Mice.

This study aimed to formulate Kappaphycus alvarezii compound powder containing Kappaphycus alvarezii powder (KP), cooked sorghum powder (SP), and longan powder (LP); which was evaluated for its therapeutic effects against chemotherapy-induced intestinal mucosal injury (CIMI). Based on rheological properties, sensory evaluation, and antioxidant activity and using single factor and response surface methodology, the optimal formula to develop the compound powder was determined to be 35% KP, 30% SP, 5% LP, and 30% xylitol. Thereafter, the efficacy of the compound powder was tested by feeding BALB/c mice with diets supplemented with the Kappaphycus alvarezii compound powder (3% and 5%) for 14 consecutive days. The chemotherapeutic drug 5-fluorouracil was intraperitoneally injected (50 mg/kg) in the mice to induce CIMI for the last three consecutive days. Compared to the CIMI mice, those fed 5% Kappaphycus alvarezii compound powder (HC) showed significantly improved the intestinal injury, increased mucin-2 secretion, and reduced TNF-α, IL-1ß, IL-6, LT, and COX-2 levels. Furthermore, HC intake significantly reduced the Firmicutes-to-Bacteroidetes ratio, promoted the growth of beneficial bacteria, such as Alloprevotella, and inhibited the growth of harmful bacteria, such as Clostridium. In conclusion, HC has a protective effect against CIMI and provides a novel dietary strategy for patients undergoing chemotherapy.

Docosahexaenoic acid-rich fish oil alleviates hepatic steatosis in association with regulation of gut microbiome in ob/ob mice.

It remains to study whether docosahexaenoic acid-rich fish oil (DHA-FO) improves hepatic lipid metabolism by leptin-independent mechanisms. We used ob/ob mice as a model to investigate the effects of DHA-FO on hepatic steatosis. DHA-FO inhibited lipid droplets (LD) formation in liver of ob/ob mice. Probably because DHA-FO consumption prevented the accumulation of oleic acid, and suppressed the synthesis of triglycerides and cholesteryl esters. These beneficial effects might be concerned with the promotion of short chain fatty acids (SCFAs) production. Furthermore, DHA-FO could reverse gut bacteria dysbiosis, including increasing the abundance of SCFAs producers (e.g. Akkermansia and unclassified_Muribaculaceae), and suppressing the proliferation of conditional pathogenic bacteria, such as unclassified_Lachnospiraceae. DHA-FO also promoted colonic microbial function ("Glycerolipid metabolism") associated with lipid metabolism. As a potential ingredient for functional food, DHA-FO reduced LD accumulation, which might be associated with modulation of obesity-linked gut microbiome in ob/ob mice.

Enzymatic hydrolysate of porphyra enhances the intestinal mucosal functions in obese mice.

Intestinal mucosal immunity is important to human body; however, obesity induced by high-fat diet may bring a series of problems, such as chronic inflammation which may damage intestinal mucosal immunity. In this study, the effects of two different enzymatic hydrolysates of porphyra on the function of intestinal mucosal were explored in obese mice. The results showed that 10 consecutive weeks of high-fat dietary intake resulted in weight gain and intestinal abnormalities in C57BL/6 mice. However, the administration of enzymatic hydrolysate of porphyra effectively protected the intestinal mucosa from these injuries while reducing levels of oxidative stress (MDA, GSH, and GSH-Px). Specifically, they were found to improve small intestine morphological structure, increase growth of goblet cells and mucous, raise expression levels of lysozyme, and stimulate SIgA secretion, especially in the group administered with the enzymatic hydrolysate containing protease and polysaccharide enzyme (EHPP). The results showed that the enzymatic hydrolysates of porphyra may provide a protective measure to maintain intestinal mucosal barriers, which is beneficial to overall health. Porphyra is widely distributed all over the world. Moreover, an increasing number of studies have described its diverse biological functions. Therefore, it is necessary to find a way to develop products related to porphyra. In this study, a new type of polysaccharide enzyme of porphyra found in our previous research was used to make a clear porphyra energy drink with a lower molecular weight polysaccharide. Our findings highlighted the repaired intestinal barriers in obese bodies after the treatment with the enzymatic hydrolysate. PRACTICAL APPLICATIONS: Porphyra is widely distributed all over the world. Moreover, an increasing number of studies have described its diverse biological functions. Therefore, it is necessary to find a way to develop products related to porphyra. In this study, a new type of polysaccharide enzyme of porphyra found in our previous research was used to make a clear porphyra energy drink with a lower molecular weight polysaccharide. Our findings highlighted the repaired intestinal barriers in obese bodies after the treatment with the enzymatic hydrolysate.

The risk of carrageenan-induced colitis is exacerbated under high-sucrose/high-salt diet.

As a common used food additive, the threat of carrageenan to colon health is controversial, and is inseparable from personal eating habits. However, no detailed descriptions are available concerning the influence of different dietary patterns on the risk of carrageenan-induced colitis. In this study, we explored the risk of κ-carrageenan-induced colitis under high-sucrose or high-salt diet in mice. Intervention with carrageenan under high-sucrose diet significantly reduced colon length and induced more serious deepening of the crypts. In addition, the intake of carrageenan under high-sucrose/high-salt diet induced more serious goblet cell reduction and increased intestinal permeability. 16S rRNA sequencing and LC-MS based metabonomic approaches were conducted to explore the changes of gut microbiota and metabolites. It was found that the intake of carrageenan under high-sucrose/high-salt diet significantly reduced the abundance of anti-inflammatory bacterium and increased the abundance of harmful bacterium, which was significantly related to the decrease of anti-inflammatory metabolites in colon, such as methyl caffeate, spermine, oleanolic acid and senecionine. Overall, high-sucrose or high-salt diet increased the risk of carrageenan-induced colitis. This reminds us to maintain good eating habits, do not prefer high-sugar or high-salt foods, and try not to consume large amounts of carrageenan continuously to maintain gut health.

The improvement effect of astaxanthin-loaded emulsions on obesity is better than that of astaxanthin in the oil phase.

Emulsion-based delivery systems have been reported to improve the solubility, stability and bioavailability of astaxanthin. In this study, the ability of astaxanthin-loaded emulsions (AL) to ameliorate obesity induced by a high-fat and high-sucrose diet was explored, using astaxanthin in the oil phase (ASTA) as a comparison. After the administration of AL, ASTA (30 mg per kg body weight), or saline on normal or obese mice for 4 weeks, the body fat accumulation levels, hepatic lipid contents and hepatic fatty acid profiles were detected, and AL showed better anti-obesity properties than ASTA. In an acute feeding experiment, it was first observed that the astaxanthin concentration of AL was higher than that of ASTA in the blood and liver of obese mice. What's more, AL altered the microbial co-occurrence patterns in obese mice. Some gut microbial modules that were significantly correlated with obesity-related physiological parameters were identified. Overall, the improvement effect of AL on obesity is better than that of ASTA due to their higher oral absorbability and modulating effects on the gut microbiota, and we suggest AL as a more suitable astaxanthin product type for obese bodies.

Fucoxanthin-loaded nanoparticles composed of gliadin and chondroitin sulfate: Synthesis, characterization and stability.

In this study, the fucoxanthin (FUC)-loaded gliadin nanoparticles (Gli NPs) stabilized by chondroitin sulfate (ChS) were fabricated. Results showed that the particle size and turbidity of Gli-ChS NPs were highly pH-dependent. Hydrogen bond, electrostatic interaction and hydrophobic interaction were involved in the formation of Gli-ChS NPs. The surface hydrophobicity of Gli NPs decreased remarkably after coating with ChS. FUC-Gli-ChS NPs increased the stability of FUC against heating and ultraviolet (UV) irradiation. Adding ChS to FUC-Gli NPs enhanced their stabilities to ionic strength and thermal treatment, especially in an acidic environment. Furthermore, FUC-loaded Gli-ChS NPs inhibited the FUC release in simulated gastric fluid (SGF), while enhanced the release of FUC in simulated intestinal fluid (SIF) and simulated colonic fluid (SCF). In summary, this work has important practical significance for the development of Gli NPs as nano-delivery systems for FUC or other hydrophobic compounds.