Dietary açai modulates ROS production by neutrophils and gene expression of liver antioxidant enzymes in rats

Açai (Euterpe oleracea Mart.) has recently emerged as a promising source of natural antioxidants. Because increased oxidative stress and impaired antioxidant defense mechanisms are important factors in the development of diabetic complications and many health claims have been reported for açai, the present study was undertaken to evaluate the possible protective effects of açai on the production of reactive oxygen species by neutrophils and on the liver antioxidant defense system in control and streptozotocin-induced diabetic rats. Diet supplementation with 2% açai was found to increase mRNA levels for gamma-glutamylcysteine synthetase and glutathione peroxidase in liver tissue and to decrease reactive oxygen species production by neutrophils. Compared to control animals, diabetic rats exhibited lower levels of mRNA coding for Zn-superoxide dismutase, glutathione peroxidase and gamma-glutamylcysteine synthetase and higher levels of reactive oxygen species production by neutrophils, thiobarbituric acid-reactive substances and carbonyl proteins in hepatic tissues. Although açai supplementation was not effective in restore gene expression of antioxidant enzymes in diabetic rats, it showed a protective effect, decreasing thiobarbituric acid-reactive substances levels and increasing reduced glutathione content in the liver. These findings suggest that açai can modulate reactive oxygen species production by neutrophils and that it has a significant favorable effect on the liver antioxidant defense system under fisiological conditions of oxidative stress and partially revert deleterious effects of diabetes in the liver

Protective Effect of Baccharis trimera Extract on Acute Hepatic Injury in a Model of Inflammation Induced by Acetaminophen

Background. Acetaminophen (APAP) is a commonly used analgesic and antipyretic. When administered in high doses, APAP is a clinical problem in the US and Europe, often resulting in severe liver injury and potentially acute liver failure. Studies have demonstrated that antioxidants and anti-inflammatory agents effectively protect against the acute hepatotoxicity induced by APAP overdose. Methods. The present study attempted to investigate the protective effect of B. trimera against APAP-induced hepatic damage in rats. The liver-function markers ALT and AST, biomarkers of oxidative stress, antioxidant parameters, and histopathological changes were examined. Results. The pretreatment with B. trimera attenuated serum activities of ALT and AST that were enhanced by administration of APAP. Furthermore, pretreatment with the extract decreases the activity of the enzyme SOD and increases the activity of catalase and the concentration of total glutathione. Histopathological analysis confirmed the alleviation of liver damage and reduced lesions caused by APAP. Conclusions. The hepatoprotective action of B. trimera extract may rely on its effect on reducing the oxidative stress caused by APAP-induced hepatic damage in a rat model. General Significance. These results make the extract of B. trimera a potential candidate drug capable of protecting the liver against damage caused by APAP overdose

Differential expression of iron metabolism proteins in diabetic and diabetic iron-supplemented rat liver.

Diabetes mellitus is associated with altered iron homeostasis that can potentially effect reactive oxygen species generation and contribute to diabetes-related complications. We investigated, by quantitative polymerase chain reaction, whether the expression of liver hepcidin, ferritin, and TfR-1 is altered in diabetes. Rats in the control (C) group received a standard diet; control iron (CI) group received a standard diet supplemented with iron; diabetic (D) group received an injection of streptozotocin; and diabetic iron (DI) group received streptozotocin and the diet with iron.Animals of theDgroup showed higher levels of serum iron, increased concentration of carbonyl protein, and a decrease in antioxidant status. Group D rats showed increased hepatic expression of Trf-1 compared to the other groups. Iron supplementation reversed this increase. Hepcidin mRNA was 81% higher in DI than in C and CI rats. The results suggest that diabetes, with or without excess iron, can cause perturbations in iron status, hepcidin and Trf-1 expression

Whey protein modifies gene expression related to protein metabolism affecting muscle weight in resistance-exercised rats.

Objective: The aim of this study was to evaluate the effects of resistance exercise on the mRNA expression of muscle mammalian target of rapamycin (mTOR), muscle-specific RING finger-1 (MuRF-1), and muscle atrophy F-box (MAFbx) in the presence or absence of whey protein ingestion. We hypothesized that resistance exercise in combination with whey protein ingestion alters the gene expression of proteins related to muscle protein synthesis (mTOR) and/or degradation (MuRF-1 and MAFbx), thus affecting muscle weight gain in rats. Methods: Thirty-two male Fischer rats were randomly assigned to the following four experimental groups (n ¼ 8/group): Control sedentary, control exercised, whey protein sedentary, and whey protein exercised. Exercise consisted of inducing the animals to perform sets of jumps for 8 wk. Body weight gain, muscle weights, food intake, and feeding efficiency were evaluated. Gene expressions were analyzed by quantitative real-time reverse transcription polymerase chain reaction. Statistical evaluation was performed using a two-way analysis of variance with a Tukey post hoc test. Results: Whey protein exercised rats exhibited higher body and muscle weight gain compared with control-exercised rats (P ¼ 0.032). The expression of mTOR was reduced by exercise but increased when whey protein was consumed as a dietary protein (P ¼ 0.005). MuRF-1 expression was reduced by exercise (P < 0.001), whereas MAFbx was reduced only by whey protein ingestion (P ¼ 0.008) independent of exercise. Conclusions: A reduction in MAFbx gene transcription induced by whey protein and the interaction between exercise and whey protein ingestion on mTOR gene expression contributed significantly to differences in body and muscle weight gain

Diet supplementation with beta-carotene improves the serum lipid profile in rats fed a cholesterol-enriched diet.

The present study investigated the underlying mechanism associated with the hypocholesterolemic activity of beta-carotene by examining its effects on the serum lipid profile, fecal cholesterol excretion, and gene expression of the major receptors, enzymes, and transporters involved in cholesterol metabolism. Female Fischer rats were divided into three groups and were fed either a control or a hypercholesterolemic diet supplemented or not supplemented with 0.2 % betacarotene. After 6 weeks of feeding, blood, livers, and feces were collected for analysis, and quantitative realtime polymerase chain reaction (qRT-PCR) was performed. Dietary supplementation with 0.2 % betacarotene decreased serum total cholesterol, non-HDL cholesterol, the atherogenic index, and hepatic total lipid and cholesterol contents. These changes were accompanied by an increase in the total lipid and cholesterol contents excreted in the feces. The qRT-PCR analyses demonstrated that the hypercholesterolemic diet promoted a decrease in the gene expression of sterol regulatory element-binding protein 2, 3-hydroxy-3-methylglutaryl CoA reductase, and low-density lipoprotein receptor and an increase in the gene expression of peroxisome proliferator-activated receptor α and cholesterol-7ahydroxylase. The expression of these genes and gene expression of ATP-binding cassette subfamily G transporters 5and 8 were unaffected by beta-carotene supplementation. In conclusion, the decrease in serum cholesterol and the elevation of fecal cholesterol obtained following beta-carotene administration indicate that this substance may decrease cholesterol absorption in the intestine and increase cholesterol excretion into the feces without a direct effect on the expression of cholesterol metabolism genes

Identification, characterization and quantification of xanthones from Fridericia formosa leaves extract with antiviral activity

Abstract Fridericia formosa (Bureau) L.G. Lohmann (Bignonaceae) is a neotropical liana species found in the Cerrado biome in Brazil. It has been of great interest to the scientific community due to its potential as a source of new antivirals, including xanthones derived from mangiferin. In this context, the present study aimed to characterize and quantify the xanthones present in the ethanol extract of this species using high performance liquid chromatography. Additionally, the antiviral activity against Chikungunya, Zika, and Mayaro viruses was evaluated. The chromatographic analyses partially identified twenty-six xanthones, among which only fourteen had already been described in the literature. The xanthones mangiferin, 2′-O-trans-caffeoylmangiferin, and 2′-O-trans-coumaroylmangiferin, are present in higher quantities in the extract, at concentrations of 9.65%, 10.68%, and 3.41% w/w, respectively. In antiviral assays, the extract inhibited the multiplication cycle only for the Mayaro virus with a CE50 of 36.1 μg/mL. Among the isolated xanthones, 2′-O-trans-coumaroylmangiferin and 2′-O-trans-cinnamoylmangiferin inhibited the viral cytopathic effect with CE50 values of 180.6 and 149.4 μg/mL, respectively. Therefore, the extract from F. formosa leaves, which has a high content of xanthones, has antiviral potential and can be a source of new mangiferin derivatives

Protective Effect of Baccharis trimera Extract on Acute Hepatic Injury in a Model of Inflammation Induced by Acetaminophen

Background. Acetaminophen (APAP) is a commonly used analgesic and antipyretic. When administered in high doses, APAP is a clinical problem in the US and Europe, often resulting in severe liver injury and potentially acute liver failure. Studies have demonstrated that antioxidants and anti-inflammatory agents effectively protect against the acute hepatotoxicity induced by APAP overdose. Methods. The present study attempted to investigate the protective effect of B. trimera against APAP-induced hepatic damage in rats. The liver-function markers ALT and AST, biomarkers of oxidative stress, antioxidant parameters, and histopathological changes were examined. Results. The pretreatment with B. trimera attenuated serum activities of ALT and AST that were enhanced by administration of APAP. Furthermore, pretreatment with the extract decreases the activity of the enzyme SOD and increases the activity of catalase and the concentration of total glutathione. Histopathological analysis confirmed the alleviation of liver damage and reduced lesions caused by APAP. Conclusions. The hepatoprotective action of B. trimera extract may rely on its effect on reducing the oxidative stress caused by APAP-induced hepatic damage in a rat model. General Significance. These results make the extract of B. trimera a potential candidate drug capable of protecting the liver against damage caused by APAP overdose