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.

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.

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.

Sun-Dried and Air-Dried Kappaphycus alvarezii Attenuates 5-Fluorouracil-Induced Intestinal Mucositis in Mice.

5-fluorouracil (5-FU)-induced intestinal mucositis (IM) often makes chemotherapy patients suffer from physical and psychological suffering. Kappaphycus alvarezii (KA) is known for its potent multiple biological activities from decades. In the current study, we explored the effect of sun-dried and air-dried Kappaphycus alvarezii as a whole food supplement on 5-FU-induced IM. Diets supplemented with sun-dried Kappaphycus alvarezii (SKA, 3%), air-dried Kappaphycus alvarezii (AKA, 3%), and 5-aminosalicylic acid (0.005%) for consecutive14 days. While intraperitoneal injection of 5-FU (50 mg/kg) induced IM for last three consecutive days, and IM was assessed by the disease activity index (DAI) and inflammatory cytokine levels. Pretreatment of KA could alleviate phenotypic index, inhibit the increase of DAI, and reverse villus/crypt ratio. On the 14th day, AKA significantly increased the weight growth rate of the mice. The intervention of SKA significantly reduced the level of TNF-α and IL-1ß (P < 0.01, P < 0.01), while the intervention of AKA significantly inhibited the level of TNF-α, IL-1ß, and LT (P < 0.01, P < 0.01, P < 0.001). Therefore, these results showed that KA as a whole food supplement might be prevent the 5-FU-induced IM. For the first time suggest that the use of AKA might be more effective than SKA despite exact mechanism still needs further study.

Effects of curcumin-mediated photodynamic treatment on lipid degradation of oysters during refrigerated storage.

BACKGROUND: Oyster's lipid degradation leads to a decrease in edible and nutritional value. Curcumin-mediated photodynamic treatment (PDT) is an innovative non-thermal technology, although evaluation of the oyster's lipid degradation has been scarce. In the present study, we investigated peroxide value, thiobarbituric acid reactive substance, triacylglycerol and free fatty acids to evaluate the effect of curcumin-mediated PDT on lipid degradation of oysters during refrigerated storage. RESULTS: The results showed that curcumin-mediated PDT could delay oyster's lipid degradation. Next, the activities of enzymes were detected to determine the mechanisms behind the effects of curcumin-mediated PDT. It was revealed that the activities of lipase, phospholipase A2 (PLA2 ), phospholipase C (PLC), phospholipase D (PLD) and lipoxygenase (LOX) were significantly inhibited after curcumin-mediated PDT (P < 0.05). Furthermore, 16 s rRNA analysis established that the relative abundances of Pseudoalteromonas and Psychrilyobacter were reduced by 51.58% and 43.82%, respectively, after curcumin-mediated PDT. CONCLUSION: Curcumin-mediated PDT could delay oyster's lipid degradation by inhibiting the activities of lipase, PLA2 , PLC, PLD and LOX, as well as by changing the oyster's microbial composition, reducing the relative abundance of Pseudoalteromonas and Psychrilyobacter. © 2021 Society of Chemical Industry.

Food-grade carrageenans and their implications in health and disease.

Food additives, often used to guarantee the texture, shelf-life, taste, and appearance of processed foods, have gained widespread attention due to their increased link to the growing incidence of chronic diseases. As one of the most common additives, carrageenans have been used in human diets for hundreds of years. While classified as generally recognized as safe (GRAS) for human consumption, numerous studies since the 1980s have suggested that carrageenans, particularly those with random coil conformations, may have adverse effects on gastrointestinal health, including aggravating intestinal inflammation. While these studies have provided some evidence of adverse effects, the topic is still controversial. Some have suggested that the negative consequence of the consumption of carrageenans may be structure dependent. Furthermore, pre-existing conditions may predispose individuals to varied outcomes of carrageenan intake. In this review, structure-function relationships of various carrageenans in the context of food safety are discussed. We reviewed the molecular mechanisms by which carrageenans exert their biological effects. We summarized the findings associated with carrageenan intake in animal models and clinical trials. Moreover, we examined the interactions between carrageenans and the gut microbiome in the pathogenesis of gastrointestinal disorders. This review argues for personalized guidance on carrageenan intake based on individuals' health status. Future research efforts that aim to close the knowledge gap on the effect of low-dose and chronic carrageenan intake as well as interactions among food additives should be conducive to the improved safety profile of carrageenans in processed food products.

The role of gut microbiota in the resistance to obesity in mice fed a high fat diet.

The prevalence of diet induced obesity (DIO) is a huge threat to global health. Differences in gut microbiota may be concerned with DIO. Sixty male C57BL/6J mice were fed with high fat diet (HFD, 45% kcal from fat) for 16 weeks. Among them, body weight, body fat rate and the lipid content in plasma or liver of six mice (Lean (L) group) were obviously lower than average levels (Fatty (F) group). These results supported that some individuals were resistant to HFD induced obesity. Using 16S rRNA analysis to investigate the role of gut microbiota in this resistance, we found several alterations associated with the resistance, such as an increase of Muribaculaceae in L group. Moreover, analysis of predicted microbial function suggested that bacteria in F group could better utilise HFD compared to L group. In conclusion, gut microbiota might play a bigger role than diet in resisting obesity, and it could be a potential target for obesity treatment.

Astaxanthin n-Octanoic Acid Diester Ameliorates Insulin Resistance and Modulates Gut Microbiota in High-Fat and High-Sucrose Diet-Fed Mice.

Astaxanthin n-octanoic acid diester (AOD) is a type of astaxanthin connecting medium-chain fatty acids with a more stable structure. In this study, we examined the role of AOD in ameliorating insulin resistance (IR) induced by a high-fat and high-sucrose diet (HFD) as well as its effect on modulating gut microbiota in mice, with free astaxanthin (AST) as a comparison. Four groups of male C57BL/6J mice (6 weeks old; n = 10 per group) were fed with a normal control diet (NC), HFD orally administered with AOD, AST (50 mg/kg body weight), or vehicle for 8 weeks. AOD improved glucose tolerance, IR, systematic and intestinal inflammation, and intestinal integrity better than AST. Further, both AOD and AST modulated gut microbiota. A significantly higher abundance of Bacteroides and Coprococcus was found in AOD than in AST, and the predicted pathway of carbohydrate metabolism was significantly impacted by AOD. Overall, AOD may play a role in alleviating IR and inflammation with the modulating effect on microbiota in HFD-fed mice. Our findings could facilitate the development of AOD as a bioactive nutraceutical and more stable alternative to AST.

Mechanism of neoagarotetraose protects against intense exercise-induced liver injury based on molecular ecological network analysis.

Here we have explored the effect of neoagarotetraose (NAT) on liver injury caused by intense exercise. Our results showed that NAT treatment obviously decreased liver weight (p < 0.01), improved the liver morphological structure, decreased ALT level (p < 0.05) and endotoxin (LPS) (p < 0.01). In addition, NAT could regulate bile acid profiles in feces and serum of mice, which indicated the potential of liver function, suggesting that NAT was effective to relieve intense exercise-induced liver injury. NAT could regulate the expression of colon genes. NAT tended to alter the microbial composition of mice under intense exercise. We uncovered the network interactions between liver traits and microbial communities in NAT treatment mice. Interestingly, our data indicated that intense exercise-induced liver injury may be related to Clostridiales. In summary, these results demonstrated that NAT relieved liver injury induced by intense exercise may be related to gut microbiota.

Microbial Co-Occurrence Patterns and Keystone Species in the Gut Microbial Community of Mice in Response to Stress and Chondroitin Sulfate Disaccharide.

Detecting microbial interactions is essential to the understanding of the structure and function of the gut microbiome. In this study, microbial co-occurrence patterns were inferred using a random matrix theory based approach in the gut microbiome of mice in response to chondroitin sulfate disaccharide (CSD) under healthy and stressed conditions. The exercise stress disrupted the network composition and microbial co-occurrence patterns. Thirty-four Operational Taxonomic Units (OTU) were identified as module hubs and connectors, likely acting as generalists in the microbial community. Mucispirillum schaedleri acted as a connector in the stressed network in response to CSD supplement and may play a key role in bridging intimate interactions between the host and its microbiome. Several modules correlated with physiological parameters were detected. For example, Modules M02 (under stress) and S05 (stress + CSD) were strongly correlated with blood urea nitrogen levels (r = 0.90 and -0.75, respectively). A positive correlation between node connectivity of the OTUs assigned to Proteobacteria with superoxide dismutase activities under stress (r = 0.57, p < 0.05) provided further evidence that Proteobacteria can be developed as a potential pathological marker. Our findings provided novel insights into gut microbial interactions and may facilitate future endeavor in microbial community engineering.

Effect of photodynamic inactivation of Escherichia coli by hypericin.

The present study has focused on the effects of hypericin (Hyp) based photodynamic inactivation (PDI) of Escherichia coli (E. coli). To evaluate the efficiency of Hyp based PDI of E. coli, single factor experiments and response surface optimization experiment were conducted to obtain the optimum parameter values (36 µM Hyp, 5.9 J cm-2 light dose: 16.4 mW cm-2, 60 W, 260 s, 590 nm and 68 min incubation time) and finally achieved a 4.1 log CFU mL-1 decrease of E. coli. Cell-Hyp interaction and intracellular reactive oxygen species (ROS) level were detected by fluorescence spectrometric photometer. Data indicated that Hyp possessed a strong ability to bind with cells. In addition, a significant increase was observed in intracellular ROS level after Hyp-based photosensitization treatment. Therefore, Hyp-based photosensitization seems to be a promising method to efficiently inactivate E. coli. It is expected to be a safe, efficient, low cost and practical method which can be applied in the field of food safety.

The Protective and Immunomodulatory Effects of Fucoidan Against 7,12-Dimethyl benz[a]anthracene-Induced Experimental Mammary Carcinogenesis Through the PD1/PDL1 Signaling Pathway in Rats.

Fucoidan is a sulfated polysaccharide that is extracted from brown algae seaweed. This study was designed to evaluate the protective and immunomodulatory effects of dietary fucoidan on 7,12-dimethyl benz[a]anthracene (DMBA)-induced experimental mammary carcinogenesis in rats. Sixty Sprague-Dawley rats were randomly assigned to four equal groups: the control group (control group), the cancer model group (model group), and the F1 and F2 groups, which were fed fucoidan at concentrations of 200 and 400 mg/kg·body weight, respectively. We found that fucoidan treatment decreased the tumor incidence and mean tumor weight and prolonged the tumor latency. Flow cytometric analyses revealed that the number of blood natural killer cells was higher after fucoidan treatment and that the proportions of CD4 and CD8 T cells were also increased. The serum levels of interleukin (IL)-6, IL-12p40, and interferon (IFN)-γ were higher in the rats treated with fucoidan compared to those of model rats. Moreover, the percentage of CD3+ Foxp3+ regulatory T cells in the blood and the levels of IL-10 and transforming growth factor ß in the serum were lower in the rats treated with fucoidan. Furthermore, fucoidan treatment decreased the expression of Foxp3 and programmed cell death 1 ligand 1 (PDL1) in tumor tissues. The levels of p-phosphatidyl inositol kinase 3 and p-AKT in tumor tissues were also lower than those of model rats. These results suggest that a fucoidan-supplemented diet can inhibit DMBA-induced tumors in rats. This study provides experimental evidence toward elucidating the immune enhancement induced by fucoidan through the programmed cell death 1/PDL1 signaling pathway. The immunomodulatory effect is one of the possible mechanisms of the protective effect of fucoidan against mammary carcinogenesis.

Polymannuronic acid ameliorated obesity and inflammation associated with a high-fat and high-sucrose diet by modulating the gut microbiome in a murine model.

Polymannuronic acid (PM), one of numerous alginates isolated from brown seaweeds, is known to possess antioxidant activities. In this study, we examined its potential role in reducing body weight gain and attenuating inflammation induced by a high-fat and high-sucrose diet (HFD) as well as its effect on modulating the gut microbiome in mice. A 30-d PM treatment significantly reduced the diet-induced body weight gain and blood TAG levels (P2·0). PM also had a profound impact on the microbial composition in the gut microbiome and resulted in a distinct microbiome structure. For example, PM significantly increased the abundance of a probiotic bacterium, Lactobacillus reuteri (log10 LDA score>2·0). Together, our results suggest that PM may exert its immunoregulatory effects by enhancing proliferation of several species with probiotic activities while repressing the abundance of the microbial taxa that harbor potential pathogens. Our findings should facilitate mechanistic studies on PM as a potential bioactive compound to alleviate obesity and the metabolic syndrome.

The squid ink polysaccharides protect tight junctions and adherens junctions from chemotherapeutic injury in the small intestinal epithelium of mice.

Gastrointestinal mucositis and infection by chemotherapy treatment are associated with alterations in the functioning of the intestinal barrier, due to the potential damage induced by anticancer drugs on the epithelial tight junctions and adheren junction. We aimed to study the protective effect of dietary polysaccharides on chemotherapy-induced injury in the epithelial cells. In the current study, using mice that were intraperitoneally injected with 50 mg/kg cyclophosphamide for 2 days, we reveal that polysaccharides from the ink of Ommastrephes bartrami (OBP) enhanced the mRNA and protein expression levels of Occludin, zonulae occluden (ZO)-1, and E-cadherin. Immunohistochemistry staining of ZO-1 and E-cadherin confirmed the increase in the mRNA and protein levels. OBP also remarkably enhanced the mRNA expression of other tight junction proteins, ZO-2, ZO-3, claudin-2, and cingulin. Our results may have important implications in host defense, especially the immunopotentiation function of OBP on the cyclophosphamide-induced epithelial cell injury, as well as intestinal disorders involving inflammation and infection.

Establishment of a functional secretory IgA transcytosis model system in vitro for functional food screening.

A characteristic mucosal immune response involves the production of antigen-specific secretory immunoglobulin A (SIgA) antibodies. In order to study transcytosis by mimicking the SIgA secretion and to screen for SIgA secretion-promoting substances, we developed a model system of a transfected Madin-Darby canine kidney (MDCK) cell line that expresses the human polymeric immunoglobulin receptor (pIgR). We thus isolated the human dIgA (dimeric IgA)/pIgA (polymeric IgA) complex as the binding ligands. In the present study, a recombinant vector encoding the human pIgR gene was constructed and infected into MDCK cells. Following reverse transcription polymerase chain reaction (RT-PCR), immunoblotting, and immunofluorescence staining, we confirmed that pIgR was expressed in the transfectant MDCK-pIgR cells and was located at the basolateral side of the cell surface. We also confirmed the coexistence of the dIgA/pIgA complex in the IgA myeloma serum. The covalent dIgA/pIgA complex was then isolated from the serum of an IgA multiple myeloma patient using an ÄKTA purifier operation system with a HiPrep 16/60 Sephacryl S-300 HR column, in order to utilize the complex as transcytosis ligands for human pIgR. Finally, we confirmed the uptake of the isolated human dIgA/pIgA complex into MDCK-pIgR cells. We demonstrated that the human dIgA/pIgA complex was transcytosed into the apical side of the monolayer cells. Therefore, our MDCK-human pIgR cell transcytosis model is an operational system and can be used for screening functional food components that promote dIgA/pIgR transcytosis as well as SIgA secretion.

Dietary Apostichopus japonicus enhances the respiratory and intestinal mucosal immunity in immunosuppressive mice.

Although Apostichopus japonicus is recognized as a food and drug resource with significant immunomodulatory activity, its role in regulating the mucosal immunity remains unclear. This study aimed to explore the effects of dietary A. japonicus on mucosal immunity with an immunosuppressive mouse model. The expression of lysozyme, secretory immunoglobulin A(sIgA), and immunoglobulin A(IgA) as well as polymeric immunoglobulin receptor(pIgR) in respiratory and intestine organs was investigated. The results showed that A. japonicus could improve both the systematic and mucosal immunity. The expression of lysozyme, sIgA, and IgA in the respiratory organ was increased more significantly. Consumption of A. japonicus with the dose of 512 mg kg(-1), which equals to (1)/2 sea cucumber per day for adults, showed better effects. This study elucidated positive effects of A. japonicus on mucosal immunity for the first time, suggesting that moderate consumption of A. japonicus is helpful in improving mucosal immunity and preventing exogenous infection.

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.

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 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.

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.