Effects of sturgeon oil and its Pickering emulsion on the quality of sturgeon surimi gel.

This study aimed to extract sturgeon oil (SO) from the sturgeon head and apply it to sturgeon meat to produce surimi gel. The effects of SO and its Pickering emulsion on the qualities of surimi gel were investigated. The results demonstrated that Pickering emulsions improved the quality deterioration of the gel caused by the direct addition of SO, especially the soy isolate protein (SPI) emulsion and the pea isolate protein (PPI) emulsion. Pickering emulsions contributed to a more uniform and compact network structure of the gel, improved the texture properties, enhanced the freeze-thaw stability, and reduced lipid oxidation. Additionally, compared to the addition of exogenous lipids such as peanut oil and linseed oil, SO and its Pickering emulsion better maintained the characteristic flavor of sturgeon surimi gel. This study provides valuable data and feasible ideas for expanding the utilization of sturgeon by-products and developing new types of surimi gel products.

Structural and aggregation changes of silver carp myosin induced with alcohols: Effects of ethanol, 1,2-propanediol, and glycerol.

This study investigated the effects of ethanol, 1,2-propanediol, and glycerol on the structure and aggregation behavior of silver carp (Hypophthalmichthys molitrix) myosin. All alcohols induced extensive alteration in the tertiary structure of myosin. Both ethanol and 1,2-propanediol further promoted an increase in the content of ß-sheets in myosin and induced myosin aggregation. While glycerol had almost no impact on the secondary structure of myosin. Molecular dynamics simulations revealed that increasing the concentration of ethanol and 1,2-propanediol affected the overall structural changes in the myosin heavy chain (MHC), while glycerol exerted a more pronounced effect on the MHC tail when compared to the MHC head. Disruption of the hydration layers induced by ethanol and 1,2-propanediol contributed to local structural changes in myosin. Glycerol at a concentration of 20% induced the formation of a larger hydration layer around the MHC tail, which facilitated the stabilization of the protein structure.

Human umbilical cord-derived mesenchymal stem cells ameliorate liver fibrosis by improving mitochondrial function via Slc25a47-Sirt3 signaling pathway.

Chronic Liver fibrosis may progress to liver cirrhosis and hepatocellular carcinoma (HCC), hence cause a substantial global burden. However, effective therapies for blocking fibrosis are still lacking. Although mesenchymal stem cells (MSCs) have been proven beneficial to liver regeneration after damage, the underlying mechanism of their therapeutic effects are not fully understood. Oxidative stress and mitochondrial functionality alteration directly contributes to the hepatocyte apoptosis and development of liver fibrosis. This study aims to elucidate the mechanism by which hUC-MSC alleviates liver fibrosis and mitochondrial dysfunction. RNA-sequencing was performed to characterize the transcriptomic changes after implantation of hUC-MSCs in mice with liver fibrosis. Next, western blot, RT-PCR, immunohistochemical and immunofluorescence staining were used to evaluate the expression of different genes in vitro and in vivo. Additionally, mitochondrial morphological and dynamic changes, ROS content, and ATP production were examined. Slc25a47, a newly identified liver-specific mitochondrial NAD+ transporter, was notably reduced in CCl4-treated mice and H2O2-stimulated hepatocytes. Conversely, hUC-MSCs increased the Slc25a47 expression and NAD+ level within mitochondria, thereby enhanced Sirt3 protein activity and alleviated mitochondrial dysfunction in the liver. Furthermore, Slc25a47 knockdown could partially abrogate the protective effects of hUC-MSCs on H2O2-induced mitochondrial fission and oxidative stress in hepatocytes. Our study illustrates that Slc25a47 is a key molecular for hUC-MSCs to improve liver fibrosis and regulates mitochondrial function through Sirt3 for the first time, and providing a theoretical basis for the clinical translation of hUC-MSCs transplantation in the treatment of patients with liver fibrosis/cirrhosis.

Human umbilical cord mesenchymal stem cells inhibit liver fibrosis via the microRNA-148a-5p/SLIT3 axis.

BACKGROUND: Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) have garnered considerable attention as prospective modalities of treatment for liver fibrosis (LF). The inhibition of hepatic stellate cell (HSC) activation underlies the anti-fibrotic effects of hUC-MSCs. However, the precise mechanism by which hUC-MSCs impede HSC activation remains unclarified. We aimed to elucidate the intrinsic mechanisms underlying the therapeutic effects of hUC-MSCs in LF patients. METHODS: Mice with liver cirrhosis induced by carbon tetrachloride (CCl4) were used as experimental models and administered hUC-MSCs via tail-vein injection. The alterations in inflammation and fibrosis were evaluated through histopathological examinations. RNA sequencing (RNA-seq) and bioinformatics analysis were then conducted to investigate the therapeutic mechanism of hUC-MSCs. Finally, an in-vitro experiment involving the co-cultivation of hUC-MSCs or hUC-MSC-derived exosomes (MSC-Exos) with LX2 cells was performed to validate the potential mechanism underlying the hepatoprotective effects of hUC-MSCs in LF patients. RESULTS: hUC-MSC therapy significantly improved liver function and alleviated LF in CCl4-induced mice. High-throughput RNA-Seq analysis identified 1142 differentially expressed genes that were potentially involved in mediating the therapeutic effects of hUC-MSCs. These genes play an important role in regulating the extracellular matrix. miRNA expression data (GSE151098) indicated that the miR-148a-5p level was downregulated in LF samples, but restored following hUC-MSC treatment. miR-148a-5p was delivered to LX2 cells by hUC-MSCs via the exosome pathway, and the upregulated expression of miR-148a-5p significantly suppressed the expression of the activated phenotype of LX2 cells. SLIT3 was identified within the pool of potential target genes regulated by miR-148a-5p. Furthermore, hUC-MSC administration upregulated the expression of miR-148a-5p, which played a crucial role in suppressing the expression of SLIT3, thereby palliating fibrosis. CONCLUSIONS: hUC-MSCs inhibit the activation of HSCs through the miR-148a-5p/SLIT3 pathway and are thus capable of alleviating LF.

Advancements in mesenchymal stem cell therapy for liver cirrhosis: Unveiling origins, treatment mechanisms, and current research frontiers.

Chronic liver disease inevitably progresses to liver cirrhosis, significantly compromising patients' overall survival and quality of life. However, a glimmer of hope emerges with the emergence of mesenchymal stem cells, possessing remarkable abilities for self-renewal, differentiation, and immunomodulation. Leveraging their potential, MSCs have become a focal point in both basic and clinical trials, offering a promising therapeutic avenue to impede fibrosis progression and enhance the life expectancy of individuals battling hepatic cirrhosis. This comprehensive review serves to shed light on the origin of MSCs, the intricate mechanisms underlying cirrhosis treatment, and the cutting-edge advancements in basic and clinical research surrounding MSC-based therapies for liver cirrhosis patients.

Human umbilical cord-derived mesenchymal stromal cells alleviate liver cirrhosis through the Hippo/YAP/Id1 pathway and macrophage-dependent mechanism.

BACKGROUND: Few effective anti-fibrotic therapies are currently available for liver cirrhosis. Mesenchymal stromal cells (MSCs) ameliorate liver fibrosis and contribute to liver regeneration after cirrhosis, attracting much attention as a potential therapeutic strategy for the disease. However, the underlying molecular mechanism of their therapeutic effect is still unclear. Here, we investigated the effect of human umbilical cord-derived mesenchymal stromal cells (hUC-MSCs) in treating liver cirrhosis and their underlying mechanisms. METHODS: We used carbon tetrachloride (CCl4)-induced mice as liver cirrhosis models and treated them with hUC-MSCs via tail vein injection. We assessed the changes in liver function, inflammation, and fibrosis by histopathology and serum biochemistry and explored the mechanism of hUC-MSCs by RNA sequencing (RNA-seq) using liver tissues. In addition, we investigated the effects of hUC-MSCs on hepatic stellate cells (HSC) and macrophages by in vitro co-culture experiments. RESULTS: We found that hUC-MSCs considerably improved liver function and attenuated liver inflammation and fibrosis in CCl4-injured mice. We also showed that these cells exerted therapeutic effects by regulating the Hippo/YAP/Id1 axis in vivo. Our in vitro experiments demonstrated that hUC-MSCs inhibit HSC activation by regulating the Hippo/YAP signaling pathway and targeting Id1. Moreover, hUC-MSCs also alleviated liver inflammation by promoting the transformation of macrophages to an anti-inflammatory phenotype. CONCLUSIONS: Our study reveals that hUC-MSCs relieve liver cirrhosis in mice through the Hippo/YAP/Id1 pathway and macrophage-dependent mechanisms, providing a theoretical basis for the future use of these cells as a potential therapeutic strategy for patients with liver cirrhosis.

Recent advances in the immunomodulation mechanism of mesenchymal stem cell therapy in liver diseases.

Liver fibrosis, acute liver injury or liver failure, liver tumors, and immune rejection after liver transplantation are common clinical liver diseases. Immune responses are the key to determining the prognosis of liver diseases. Liver transplantation could be the last resort for patients with liver failure. However, the use of liver transplantation is limited because of the scarcity of organ donors, immunological rejection in recipients, and high cost. Mesenchymal stem cells (MSCs) are pluripotent adult stem cells with extensive anti-inflammatory and immunomodulation effects. MSCs can be effectively used for treating liver diseases but without the limitations that are associated with liver transplantation. Therefore, several clinical trials have utilized MSCs for the treatment of refractory liver diseases and the related mechanism is increasingly being elucidated. We have mainly summarized the recent studies that focus on the immunomodulation mechanism of MSC therapy in liver diseases. Further, we have presented our insights on the prospects of using MSCs in the treatment of liver diseases.

Ameliorative effects of L-arginine? On heat-induced phase separation of Aristichthys nobilis myosin are associated with the absence of ordered secondary structures of myosin.

This investigation aimed to study the potential mechanism of L-arginine (L-Arg) on the heat-induced phase separation phenomenon of myosin from the perspective of conformational changes of myosin. L-Arg ameliorated the phase separation of myosin after a two-step heating procedure via suppression of heat-induced aggregation of myosin. The effect of L-Arg on the heating of myosin at high temperatures (75-85 °C) was more pronounced than that in the setting stage (35-45 °C), suggesting that the ameliorative effects of L-Arg on the heat-induced phase separation of myosin are mainly attributed to the inhibition of rod-rod cross-linking between denatured myosin molecules. Additionally, L-Arg without pH modification exhibited an increased ability to suppress the gelation of myosin compared with pH modification, indicating that both pH effects and the particular structure of L-Arg play noticeable roles in the suppression of myosin gelation. Far-UV circular dichroism, intrinsic fluorescence spectroscopy and differential scanning calorimetry demonstrated that L-Arg induced the absence of ordered secondary structures of myosin molecules, especially ß-sheets, and thus generated a looser protein structure, which may represent the dominant suppression mechanisms of L-Arg on the heat-induced aggregation of myosin. This work provided support for the use of L-Arg as a food additive, and the results of this study will be attractive to the meat and beverage products.

Use of l-arginine-assisted ultrasonic treatment to change the molecular and interfacial characteristics of fish myosin and enhance the physical stability of the emulsion.

The effects of l-arginine (Arg)-assisted ultrasonic treatment on the molecular and interfacial characteristics of myosin and emulsifying properties of the emulsion were evaluated to ascertain the underlying mechanism in improving the emulsion stability. Ultrasonication induced the exposure of residues of native myosin, which was increased by the addition of Arg (40 mM). Furthermore, in terms of emulsions containing Arg, the higher the ultrasonication intensity was, the greater the increase in adsorbed protein (from 15.43 ± 0.28% to 50.49 ± 1.65%) and π value, and the decrease in droplet sizes (from 4098 nm to 2324 nm) (P < 0.05). Moreover, the increase in the ordered structures of interfacial myosin induced by Arg and ultrasonication favoured the formation of a protein gelation network. In summary, Arg-assisted ultrasonic treatment improved the stability of the emulsion by inducing the exposure of native myosin and facilitating the formation of ordered structures of interfacial myosin.

[Determination of alditols in wine by gas chromatography-mass spectrometry after acetate derivatization].

The acetate derivatization of alditols for determining alditol level in wine by gas chromatography (GC)-mass spectrometry (MS) has been developed. The wine sample was mixed with pyridine and centrifuged at 5,000 r/min at the temperature of 4 degrees C for 10 min. After filtration with organic phase membrane, the supernatant was derivatized with acetic anhydride, and then dehydrated with anhydrous sodium sulfate. The GC separation was performed on a DB-5MS capillary column. The alditols were determined by MS in selected ion monitoring (SIM) mode and quantified by external standard method. The calibration curves showed good linearities in the range of 0.019 - 1.25 mg/L except for lactitol (0.039 - 2.50 mg/L) with the correlation coefficients greater than 0.99. The limits of quantification (S/N= 10) of erythritol, xylitol, D-mannitol, sorbitol, galactitol and lactitol were 0.17, 0.29, 0.43, 0.46, 0.47 and 2.88 mg/L respectively. The limits of detection (S/N = 3) were 0.05, 0.08, 0.13, 0.14, 0.14 and 1.38 mg/L respectively. The recoveries of alditols spiked in the wine at two levels of 40 mg/L and 80 mg/L were ranged from 80.15% to 108.75% with the relative standard deviations (RSDs) of 2.16% - 6.97%. The sensitivity, accuracy and precision of the method can meet the technical standard. The method can be applied to the rapid determination of alditols in wine.

Effect of superfine grinding on antidiabetic activity of bitter melon powder.

The antidiabetic activities of bitter melon powders produced with lyophilization/superfine grinding and hot air drying/normal grinding were investigated in vivo for selecting a suitable bitter melon processing procedure. After a five-week treatment, bitter melon lyophilized superfine grinding powder (BLSP) had a higher antidiabetic activity with reducing fasting blood glucose levels from 21.40 to 12.54 mmol/L, the serum insulin levels from 40.93 to 30.74 mIU/L, and restoring activities of SOD compared with those in the bitter melon hot air drying powder (BAP) treated group. Furthermore, BLSP protected pancreatic tissues including islet beta cells and reduced the loss of islet cells. Combined with the difference of compositions in BLSP and BAP, it could be concluded that superfine grinding and lyophilization processes were beneficial for presenting the antidiabetic activity, which will provide a reference for direct utilization of bitter melon as a suitable functional food to relieve symptoms of diabetes.

[Disseminated Penicillium marneffei infection associated with AIDS, report of a case].

OBJECTIVE: To explore the clinical and laboratory features of disseminated Penicillium marneffei infection in patients with AIDS. METHODS: The HIV antibody in serum was assayed by both enzyme immunoassay (EIA) and Western immunoblot (WIB) methods. Morphology of the pathogenic fungus in smear and biopsy specimens of bone marrow was observed. The fungus was isolated from the patient's skin lesion and inoculated into the abdominal cavities of 2 rats and 2 mice. Twenty days later the rats and mice were killed and their viscera were taken out. Blood from the organs were cultured in Sabourand glucose agar at 25 degrees C and 37 degrees C. The colonies were observed. The morphology of the fungus was observed by microscopy and scanning electron microscopy. RESULTS: The most common clinical manifestations of Penicilium marneffei infection were fever, weight loss, anemia, papular skin lesion, hepatosplenomegaly, and lymphadenectasis. Yeast-like cells were found in the culture at 37 degrees C or in tissues. The fungi outside the host cells were elongated, often curved, sausage-like and with clear central septi. When cultured at 25 degrees C, the fungus was mycelia-like and produced a characteristic red pigment, diffusing into the medium. CONCLUSION: Disseminated Penicilliosis marneffei is one of the most important opportunistic infections in patients with AIDS in Southeast Asia and the southern part of China. Since there is no specific clinical manifestation for Penicillium marneffei infection, it is often misdiagnosed. Definite diagnosis requires culture of the pathogenic fungus from clinical specimens. The fungus is thermally dimorphic, produces red pigment, and is sausage-form with clear central septum outside the host cell. Amphotericin B and itraconazole are effective in treating Penicilliosis marneffei.