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Plasma total bile acids and LCA were relatively high in these mice. These results indicate that VDR deletion influences CDCA metabolism. VDR may play a role in the excretion of excess bile acids.The purpose of this study was to clarify factors affecting the browning of a model processed cheese during storage. Model processed cheese samples (pH 4.5-6.0) which were composed of sugars (galactose, glucose, or lactose; 0-1.8%), amino acids (0-2.8%), sodium caseinate (26.0-31.2%), fat from butter (22.0-28.5%), water (44.1%), emulsifying salts (trisodium citrate, disodium tartrate dihydrate, or disodium hydrogen phosphate; 0 or 1.4%), and salt (0-5.0%) were prepared. Each model processed cheese was stored at 50ºC for 4-7 d. The L*-, a*-, and b*-values of model cheese samples before and after storage were measured and the ΔE-value was calculated to estimate the browning. All model cheese samples turned brown during storage. The ΔE-value strongly correlated with the concentration of galactose (r=0.99), and pH (r=0.94), respectively. The galactose-added model cheese turned more intensively brown than glucose or lactose-added ones. The browning was not dependent on the amount of free amino acids, but on the amount of added sodium caseinate. The browning was repressed by the addition of 1 to 3% of NaCl. The model cheese added with disodium hydrogen phosphate as an emulsifying salt turned more intensively brown than those added with disodium tartrate dihydrate or trisodium citrate. The ΔE-values of model cheese samples containing galactose strongly correlated with the decrease in galactose. These results showed that galactose was one of the most important factors for regulating the browning of processed cheese during storage and that the browning was also dependent on pH, protein, NaCl, and an emulsifying salt.Glutathione, the most abundant intracellular antioxidant, protects cells against reactive oxygen species induced oxidative stress and regulates intracellular redox status. We previously demonstrated that yellow Chinese chive (ki-nira) increased the intracellular glutathione levels. Acetaminophen (APAP) is a commonly used analgesic. However, an overdose of APAP causes severe hepatotoxicity via depletion of the hepatic glutathione. In this study, we investigated the hepatoprotective effects of yellow Chinese chive extract (YCE) against APAP-induced hepatotoxicity in mice. YCE (25 or 100 mg/kg) was administered once daily for 7 d, and then APAP (700 mg/kg) was injected at 6 h before the mice were sacrificed. APAP treatment markedly increased the serum biological markers of liver injury such as alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase. Pretreatment with YCE significantly prevented the increases in the serum levels of these enzymes. Histopathological evaluation of the livers also revealed that YCE prevented APAP-induced centrilobular necrosis. Pretreatment with YCE dose-dependently elevated glutathione levels, but the difference was not significant. Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a critical role in APAP-induced hepatotoxicity by regulating the antioxidant defense system. ADT-007 inhibitor Therefore, we investigated the expression of Nrf2 and its target antioxidant enzyme. YCE led to an increased expression of Nrf2 and its target antioxidant enzymes, NAD(P)H quinone oxidoreductase 1 (NQO1), glutathione peroxidase (GPx), cystine uptake transporter (xCT), especially hemeoxygenase-1 (HO-1) in mice livers. These results suggest that YCE could induce HO-1 expression via activation of the Nrf2 antioxidant pathway, and protect against APAP-induced hepatotoxicity in mice.Calorie restriction (CR) by 30-40% decreases morbidity of age-related diseases and prolongs the lifespan of various laboratory animal species. Taurine (2-aminoethanesulfonic acid) is an important nutrient for lipid metabolism as it conjugates bile acids. Here, we investigated how taurine supplementation induces effects similar to the CR beneficial effects. Sprague Dawley rats were fed a diet containing different taurine concentrations (0, 0.5, 1.0, 3.0, 5.0%) to analyze the effects on growth, blood, and hepatic parameters. Rats fed a 5% taurine-supplemented diet showed a significant decrease in visceral fat weight, compared with control rats. Moreover, there were significant decreases in the serum total cholesterol, hepatic cholesterol and triglyceride concentrations in the taurine-supplemented groups compared with the control group in a dose-dependent manner. These results were associated with decreased mRNA expression of fatty acid synthase, and increased mRNA expression of carnitine palmitoyltransferase 1α. C57BL/6 mice were fed a 5.0% taurine-supplemented diet, and their response to 3-nitropropionic acid-induced oxidative stress was analyzed. The rate of weight loss due to oxidative stress decreased and the survival rate significantly increased in the taurine-supplemented groups compared with the control group. Finally, cells were treated with 100 μM taurine and their resistance to UV-induced oxidative stress was analyzed. We found that the p53-Chk1 pathway was less activated in taurine-treated cells compared with control cells. Furthermore, damage to cells evaluated by oxidative stress indicators revealed a reduction in oxidative damage with taurine treatment. These findings suggest that taurine partially acts as a CR mimetic.The terrestrial filamentous cyanobacterium, Nostoc commune, has been used as a food source in many countries, especially countries in Asia. In this study, N. commune-derived aqueous extracts were evaluated with regard to their antioxidative and antiglycative properties. The antioxidative activity was significantly higher in N. commune colonies isolated from the field than in extracts from colonies cultured in the laboratory. The antioxidative compound content of extracts, including phenolic compounds and phycobiliproteins, was correlated with their antioxidative power. In addition, two mycosporine-like amino acids (MAAs), specifically detected in colonies isolated from the field, were purified. In addition to assessing their antioxidative properties, the antiglycative activity of these MAAs was also assessed. Their inhibitory effects on glycation-dependent protein cross-linking might contribute to the antiglycative power of the extract prepared from field colonies. Taken together, the results from this study revealed that N.

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